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\n \n 2020\n \n \n (4)\n \n \n

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\n \n\n \n \n Brigola, A. G.; Ottaviani, A. C.; Carvalho, D. H. T.; Oliveira, N. A.; Souza, É. N.; and Pavarini, S. C. I.\n\n\n \n \n \n \n Association between cognitive impairment and criteria for frailty syndrome among older adults.\n \n \n \n\n\n \n\n\n\n Arquivos De Neuro-Psiquiatria. January 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{brigola_association_2020,\n\ttitle = {Association between cognitive impairment and criteria for frailty syndrome among older adults},\n\tissn = {1678-4227},\n\tdoi = {10.1590/0004-282X20190138},\n\tabstract = {OBJECTIVE: The association between cognitive impairment and physical frailty has been studied in older adults. The criteria degree of frailty may be keys to associated cognitive impairment. To analyze the association between cognitive impairment and the criteria for frailty.\nMETHODS: We cross-sectionally examined data from 667 older adults (≥60 years of age) from a study entitled 'Variables associated to cognition in elderly caregivers' involving patients in an urban and rural primary healthcare center. We defined cognitive impairment based on different groups of scores on the Mini Mental State Examination, and defined frailty and prefrailty using the criteria by the Cardiovascular Health Study. We performed multinomial regression models to analyze the association between levels of frailty and cognitive impairment.\nRESULTS: Similar proportions of women (54.8\\%) and men (45.2\\%) participated in the study (mean age: 71 years old). We found cognitive impairment, prefrailty and frailty in 34, 54, and 24\\% of the participants, respectively. Concomitant cognitive impairment and frailty was found in 13\\% of them. The chances of cognitive impairment increased up to 330\\% (Odds Ratio [OR]: 4.3; 95\\% confidence interval [95\\%CI] 2.4‒7.7; p{\\textless}0.001) among frail individuals, and 70\\% (OR: 1.7; 95\\%CI 1.0‒2.8; p=0.033) among prefrail individuals compared to robust/non-frail individuals. After controlling for age, education, place of residence and functional dependence, slowness and fatigue criteria were significantly associated with cognitive impairment.\nCONCLUSION: Older adults with frailty have a greater likelihood of concomitant cognitive impairment than prefrail and robust older adults. The prevalence of cognitive impairment and frailty is consistent with data reported in literature. The present findings contribute to the investigation of cognitive frailty.},\n\tlanguage = {eng},\n\tjournal = {Arquivos De Neuro-Psiquiatria},\n\tauthor = {Brigola, Allan Gustavo and Ottaviani, Ana Carolina and Carvalho, Danilo Henrique Trevisan and Oliveira, Nathalia Alves and Souza, Érica Nestor and Pavarini, Sofia Cristina Iost},\n\tmonth = jan,\n\tyear = {2020},\n\tpmid = {32022119},\n}\n\n\n\n

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\n \n\n \n \n Kaiser, P.; Allen, N.; Delaney, J. A. C.; Hirsch, C. H.; Carnethon, M.; Arnold, A. M.; and Odden, M. C.\n\n\n \n \n \n \n The association of prediagnosis social support with survival after heart failure in the Cardiovascular Health Study.\n \n \n \n\n\n \n\n\n\n Annals of Epidemiology. January 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n\n\n\n

@article{kaiser_association_2020,\n\ttitle = {The association of prediagnosis social support with survival after heart failure in the {Cardiovascular} {Health} {Study}},\n\tissn = {1873-2585},\n\tdoi = {10.1016/j.annepidem.2019.12.013},\n\tabstract = {PURPOSE: Although social support has been shown to be associated with survival among persons with cardiovascular disease, little research has focused on whether social support, measured before the onset of heart failure, can enhance survival after diagnosis. The objective of this study was to assess the association between prediagnosis social support and postdiagnosis survival among older adults with heart failure.\nMETHODS: We obtained the data from the Cardiovascular Health Study, which included noninstitutionalized adults aged 65 years or older from four sites in the United States with primary enrollment in 1989-1990. We used two measures of social support, the Lubben Social Network Scale and the Interpersonal Support Evaluation List. The analytic data set included 529 participants with a social support measure within two years before diagnosis of heart failure.\nRESULTS: After adjustment for demographic covariates, cardiovascular risk factors, and general health status, mortality rates were lower among participants in the highest tertile of social network scores (HR 0.74, 95\\% CI: 0.59, 0.93) and the middle tertile (HR 0.73 [0.58, 0.90]), compared with the lowest tertile. Results with interpersonal support were null.\nCONCLUSIONS: These findings suggest that prediagnosis structural social support may modestly buffer heart failure patients from mortality.},\n\tlanguage = {eng},\n\tjournal = {Annals of Epidemiology},\n\tauthor = {Kaiser, Paulina and Allen, Norrina and Delaney, Joseph A. C. and Hirsch, Calvin H. and Carnethon, Mercedes and Arnold, Alice M. and Odden, Michelle C.},\n\tmonth = jan,\n\tyear = {2020},\n\tpmid = {31992494},\n\tkeywords = {Interpersonal support, Mortality, Social network},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Jensen, P. N.; Fretts, A. M.; Hoofnagle, A. N.; Sitlani, C. M.; McKnight, B.; King, I. B.; Siscovick, D. S.; Psaty, B. M.; Heckbert, S. R.; Mozaffarian, D.; Sotoodehnia, N.; and Lemaitre, R. N.\n\n\n \n \n \n \n Plasma Ceramides and Sphingomyelins in Relation to Atrial Fibrillation Risk: The Cardiovascular Health Study.\n \n \n \n\n\n \n\n\n\n Journal of the American Heart Association, 9(4): e012853. February 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{jensen_plasma_2020,\n\ttitle = {Plasma {Ceramides} and {Sphingomyelins} in {Relation} to {Atrial} {Fibrillation} {Risk}: {The} {Cardiovascular} {Health} {Study}},\n\tvolume = {9},\n\tissn = {2047-9980},\n\tshorttitle = {Plasma {Ceramides} and {Sphingomyelins} in {Relation} to {Atrial} {Fibrillation} {Risk}},\n\tdoi = {10.1161/JAHA.119.012853},\n\tabstract = {Background Ceramides exhibit multiple biological activities that may influence the pathophysiological characteristics of atrial fibrillation (AF). Whether the length of the saturated fatty acid carried by the ceramide or their sphingomyelin precursors are associated with AF risk is not known. Methods and Results Among 4206 CHS (Cardiovascular Health Study) participants (mean age, 76 years; 40\\% men) who were free of prevalent AF at baseline, we identified 1198 incident AF cases over a median 8.7 years of follow-up. We examined 8 sphingolipid species: ceramide and sphingomyelin species with palmitic acid and species with very-long-chain saturated fatty acids: arachidic; behenic; and lignoceric. In adjusted Cox regression analyses, ceramides and sphingomyelins with very-long-chain saturated fatty acids were associated with reduced AF risk (ie, per 2-fold higher ceramide with behenic acid hazard ratio, 0.71; 95\\% CI, 0.59-0.86; sphingomyelin with behenic acid hazard ratio, 0.60; 95\\% CI, 0.46-0.77). In contrast, ceramides and sphingomyelins with palmitic acid were associated with increased AF risk (ceramide with palmitic acid hazard ratio, 1.31; 95\\% CI, 1.03-1.66; sphingomyelin with palmitic acid hazard ratio, 1.73; 95\\% CI, 1.18-2.55). Associations were attenuated with adjustment for NT-proBNP (N-terminal pro-B-type natriuretic peptide), but did not differ significantly by age, sex, race, body mass index, or history of coronary heart disease. Conclusions Our findings suggest that several ceramide and sphingomyelin species are associated with incident AF, and that these associations differ on the basis of the fatty acid. Ceramides and sphingomyelins with palmitic acid were associated with increased AF risk, whereas ceramides and sphingomyelins with very-long-chain saturated fatty acids were associated with reduced AF risk.},\n\tlanguage = {eng},\n\tnumber = {4},\n\tjournal = {Journal of the American Heart Association},\n\tauthor = {Jensen, Paul N. and Fretts, Amanda M. and Hoofnagle, Andrew N. and Sitlani, Colleen M. and McKnight, Barbara and King, Irena B. and Siscovick, David S. and Psaty, Bruce M. and Heckbert, Susan R. and Mozaffarian, Dariush and Sotoodehnia, Nona and Lemaitre, Rozenn N.},\n\tmonth = feb,\n\tyear = {2020},\n\tpmid = {32019406},\n\tkeywords = {atrial fibrillation, biomarker, epidemiology, lipid metabolites, lipids},\n\tpages = {e012853},\n}\n\n\n\n\n\n\n\n

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\n \n\n \n \n Lee, Y.; Lai, H. T. M.; de Oliveira Otto, M. C.; Lemaitre, R. N.; McKnight, B.; King, I. B.; Song, X.; Huggins, G. S.; Vest, A. R.; Siscovick, D. S.; and Mozaffarian, D.\n\n\n \n \n \n \n Serial Biomarkers of De Novo Lipogenesis Fatty Acids and Incident Heart Failure in Older Adults: The Cardiovascular Health Study.\n \n \n \n\n\n \n\n\n\n Journal of the American Heart Association, 9(4): e014119. February 2020.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{lee_serial_2020,\n\ttitle = {Serial {Biomarkers} of {De} {Novo} {Lipogenesis} {Fatty} {Acids} and {Incident} {Heart} {Failure} in {Older} {Adults}: {The} {Cardiovascular} {Health} {Study}},\n\tvolume = {9},\n\tissn = {2047-9980},\n\tshorttitle = {Serial {Biomarkers} of {De} {Novo} {Lipogenesis} {Fatty} {Acids} and {Incident} {Heart} {Failure} in {Older} {Adults}},\n\tdoi = {10.1161/JAHA.119.014119},\n\tabstract = {Background De novo lipogenesis (DNL) is an endogenous pathway that converts excess dietary starch, sugar, protein, and alcohol into specific fatty acids (FAs). Although elevated DNL is linked to several metabolic abnormalities, little is known about how long-term habitual levels and changes in levels of FAs in the DNL pathway relate to incident heart failure (HF). Methods and Results We investigated whether habitual levels and changes in serial measures of FAs in the DNL pathway were associated with incident HF among 4249 participants free of HF at baseline. Plasma phospholipid FAs were measured at baseline, 6 years, and 13 years using gas chromatography, and risk factors for HF were measured using standardized methods. Incident HF was centrally adjudicated using medical records. We prospectively evaluated associations with HF risk of (1) habitual FA levels, using cumulative updating to assess long-term exposure, and (2) changes in FA levels over time. During 22.1 years of follow-up, 1304 HF cases occurred. After multivariable adjustment, habitual levels and changes in levels of palmitic acid (16:0) were positively associated with incident HF (interquintile hazard ratio [95\\% CI]=1.17 [1.00-1.36] and 1.26 [1.03-1.55], respectively). Changes in levels of 7-hexadecenoic acid (16:1n-9) and vaccenic acid (18:1n-7) were each positively associated with risk of HF (1.36 [1.13-1.62], and 1.43 [1.18-1.72], respectively). Habitual levels and changes in levels of myristic acid (14:0), palmitoleic acid (16:1n-7), stearic acid (18:0), and oleic acid (18:1n-9) were not associated with incident HF. Conclusions Both habitual levels and changes in levels of 16:0 were positively associated with incident HF in older adults. Changes in 16:1n-9 and 18:1n-7 were also positively associated with incident HF. These findings support a potential role of DNL or these DNL-related FAs in the development of HF.},\n\tlanguage = {eng},\n\tnumber = {4},\n\tjournal = {Journal of the American Heart Association},\n\tauthor = {Lee, Yujin and Lai, Heidi T. M. and de Oliveira Otto, Marcia C. and Lemaitre, Rozenn N. and McKnight, Barbara and King, Irena B. and Song, Xiaoling and Huggins, Gordon S. and Vest, Amanda R. and Siscovick, David S. and Mozaffarian, Dariush},\n\tmonth = feb,\n\tyear = {2020},\n\tpmid = {32020839},\n\tkeywords = {de novo lipogenesis, fatty acids, heart failure, left ventricular ejection fraction},\n\tpages = {e014119},\n}\n\n\n\n\n\n\n\n

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\n \n 2019\n \n \n (58)\n \n \n

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\n \n\n \n \n Tehrani, D. M; Fan, W.; Nambi, V.; Gardin, J.; Hirsch, C. H; Amsterdam, E.; deFilippi , C. R; Polonsky, T.; and Wong, N. D\n\n\n \n \n \n \n Trends in Blood Pressure and High-Sensitivity Cardiac Troponin-T with Cardiovascular Disease: The Cardiovascular Health Study.\n \n \n \n\n\n \n\n\n\n Am J Hypertens. June 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{tehrani_trends_2019,\n\ttitle = {Trends in {Blood} {Pressure} and {High}-{Sensitivity} {Cardiac} {Troponin}-{T} with {Cardiovascular} {Disease}: {The} {Cardiovascular} {Health} {Study}.},\n\tissn = {1941-7225},\n\tdoi = {10.1093/ajh/hpz102},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{BACKGROUND: }High-sensitivity cardiac troponin T (hs-cTnT) is individually associated with incident hypertension (HTN) and cardiovascular disease (CVD) events. We hypothesize that the increases in hs-cTnT with increases in blood pressure will be related to higher incidence of CVD.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS: }The Cardiovascular Health Study is a longitudinal cohort of older adults. Those with hs-cTnT data and CVD risk factors at baseline and follow-up (2-3 years later) were stratified based on systolic blood pressure (SBP) (optimal: {\\textless}120 mmHg, intermediate: 120-139 mmHg, elevated: {\\textgreater}=140 mmHg) and hs-cTnT (undetectable: {\\textless}5 ng/L, detectable: 5-13 ng/L, elevated: {\\textgreater}=14 ng/L) categories. SBP and hs-cTnT were classified as increased or decreased if they changed categories between exams, and stable if they did not. Cox regression evaluated incident CVD events over an average 9 year follow-up.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{RESULTS: }Among 2219 adults, 510 (23.0 \\%) had decreased hs-cTnT, 1,279 (57.6 \\%) had stable hs-cTnT, and 430 (19.4 \\%) had increased hs-cTnT. Those with increased hs-cTnT had a higher CVD risk with stable SBP (HR: 1.28 [1.04-1.57], p=0.02) or decreased SBP (HR: 1.57 [1.08-2.28], p=0.02) compared to those within the same SBP group but a stable hs-cTnT. In those with lower SBP at follow-up, there was an inverse relation between DBP and risk of CVD events in those with increased hs-cTnT (HR: 0.44 per 10 mmHg increase, p{\\textless}0.01).{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSION: }An increase in hs-cTnT over time is associated with a higher risk of CVD even when the blood pressure is stable or decreases over time.{\\textless}/p{\\textgreater}},\n\tjournal = {Am J Hypertens},\n\tauthor = {Tehrani, David M and Fan, Wenjun and Nambi, Vijay and Gardin, Julius and Hirsch, Calvin H and Amsterdam, Ezra and deFilippi, Christopher R and Polonsky, Tamar and Wong, Nathan D},\n\tmonth = jun,\n\tyear = {2019},\n}\n\n\n\n

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\n \n\n \n \n Katsumata, Y.; Nelson, P. T; Estus, S.; and Fardo, D. W\n\n\n \n \n \n \n Translating Alzheimer’s disease-associated polymorphisms into functional candidates: a survey of IGAP genes and SNPs.\n \n \n \n\n\n \n\n\n\n Neurobiol Aging, 74: 135–146. February 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{katsumata_translating_2019,\n\ttitle = {Translating {Alzheimer}’s disease-associated polymorphisms into functional candidates: a survey of {IGAP} genes and {SNPs}.},\n\tvolume = {74},\n\tissn = {1558-1497},\n\tdoi = {10.1016/j.neurobiolaging.2018.10.017},\n\tabstract = {{\\textless}p{\\textgreater}The International Genomics of Alzheimer’s Project (IGAP) is a consortium for characterizing the genetic landscape of Alzheimer’s disease (AD). The identified and/or confirmed 19 single-nucleotide polymorphisms (SNPs) associated with AD are located on non-coding DNA regions, and their functional impacts on AD are as yet poorly understood. We evaluated the roles of the IGAP SNPs by integrating data from many resources, based on whether the IGAP SNP was (1) a proxy for a coding SNP or (2) associated with altered mRNA transcript levels. For (1), we confirmed that 12 AD-associated coding common SNPs and five nonsynonymous rare variants are in linkage disequilibrium with the IGAP SNPs. For (2), the IGAP SNPs in CELF1 and MS4A6A were associated with expression of their neighboring genes, MYBPC3 and MS4A6A, respectively, in blood. The IGAP SNP in DSG2 was an expression quantitative trait loci (eQTL) for DLGAP1 and NETO1 in the human frontal cortex. The IGAP SNPs in ABCA7, CD2AP, and CD33 each acted as eQTL for AD-associated genes in brain. Our approach for identifying proxies and examining eQTL highlighted potentially impactful, novel gene regulatory phenomena pertinent to the AD phenotype.{\\textless}/p{\\textgreater}},\n\tjournal = {Neurobiol Aging},\n\tauthor = {Katsumata, Yuriko and Nelson, Peter T and Estus, Steven and Fardo, David W},\n\tmonth = feb,\n\tyear = {2019},\n\tpages = {135--146},\n}\n\n\n\n

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\n \n\n \n \n Zeki Al Hazzouri, A.; Vittinghoff, E.; Zhang, Y.; Pletcher, M. J; Moran, A. E; Bibbins-Domingo, K.; Golden, S. H; and Yaffe, K.\n\n\n \n \n \n \n Use of a pooled cohort to impute cardiovascular disease risk factors across the adult life course.\n \n \n \n\n\n \n\n\n\n Int J Epidemiol, 48: 1004–1013. 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{zeki_al_hazzouri_use_2019,\n\ttitle = {Use of a pooled cohort to impute cardiovascular disease risk factors across the adult life course.},\n\tvolume = {48},\n\tissn = {1464-3685},\n\tdoi = {10.1093/ije/dyy264},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{BACKGROUND: }In designing prevention strategies, it may be useful to understand how early and midlife cardiovascular disease risk factor (CVDRF) exposures affect outcomes that primarily occur in mid to late life. Few single US cohorts have followed participants from early adulthood to late life.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS: }We pooled four prospective cohorts that represent segments of the adult life course, and studied 15 001 White and Black adults aged 18 to 95 years at enrollment. We imputed early and midlife exposure to body mass index (BMI), glucose, lipids and blood pressure (BP). CVDRF trajectories were estimated using linear mixed models. Using the best linear unbiased predictions, we obtained person-specific estimates of CVDRF trajectories beginning at age 20 until each participant’s end of follow-up. We then calculated for each CVDRF, summary measures of early and midlife exposure as time-weighted averages (TWAs).{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{RESULTS: }In the pooled cohort, 33.7\\% were Black and 54.8\\% were female. CVDRF summary measures worsened in midlife compared with early life and varied by sex and race. In particular, systolic and diastolic BP were consistently higher over the adult life course among men, and BMI was higher among Blacks, particularly Black women. Simulation studies suggested acceptable imputation accuracy, especially for the younger cohorts. Correlations of true and imputed CVDRF summary measures ranged from 0.53 to 0.99, and agreement ranged from 67\\% to 99\\%.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSIONS: }These results suggest that imputed CVDRFs may be accurate enough to be useful in assessing the effects of early and midlife exposures on later life outcomes.{\\textless}/p{\\textgreater}},\n\tjournal = {Int J Epidemiol},\n\tauthor = {Zeki Al Hazzouri, Adina and Vittinghoff, Eric and Zhang, Yiyi and Pletcher, Mark J and Moran, Andrew E and Bibbins-Domingo, Kirsten and Golden, Sherita H and Yaffe, Kristine},\n\tyear = {2019},\n\tpages = {1004--1013},\n}\n\n\n\n

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\n \n\n \n \n Giri, A.; Hellwege, J. N; Keaton, J. M; Park, J.; Qiu, C.; Warren, H. R; Torstenson, E. S; Kovesdy, C. P; Sun, Y. V; Wilson, O. D; Robinson-Cohen, C.; Roumie, C. L; Chung, C. P; Birdwell, K. A; Damrauer, S. M; DuVall, S. L; Klarin, D.; Cho, K.; Wang, Y.; Evangelou, E.; Cabrera, C. P; Wain, L. V; Shrestha, R.; Mautz, B. S; Akwo, E. A; Sargurupremraj, M.; Debette, S.; Boehnke, M.; Scott, L. J; Luan, J.; Zhao, J.; Willems, S. M; Thériault, S.; Shah, N.; Oldmeadow, C.; Almgren, P.; Li-Gao, R.; Verweij, N.; Boutin, T. S; Mangino, M.; Ntalla, I.; Feofanova, E.; Surendran, P.; Cook, J. P; Karthikeyan, S.; Lahrouchi, N.; Liu, C.; Sepúlveda, N.; Richardson, T. G; Kraja, A.; Amouyel, P.; Farrall, M.; Poulter, N. R; Laakso, M.; Zeggini, E.; Sever, P.; Scott, R. A; Langenberg, C.; Wareham, N. J; Conen, D.; Palmer, C. N. A.; Attia, J.; Chasman, D. I; Ridker, P. M; Melander, O.; Mook-Kanamori, D. O.; Harst, P. v. d.; Cucca, F.; Schlessinger, D.; Hayward, C.; Spector, T. D; Jarvelin, M.; Hennig, B. J; Timpson, N. J; Wei, W.; Smith, J. C; Xu, Y.; Matheny, M. E; Siew, E. E; Lindgren, C.; Herzig, K.; Dedoussis, G.; Denny, J. C; Psaty, B. M; Howson, J. M M; Munroe, P. B; Newton-Cheh, C.; Caulfield, M. J; Elliott, P.; Gaziano, J M.; Concato, J.; Wilson, P. W F; Tsao, P. S; Velez Edwards, D. R; Susztak, K.; O’Donnell, C. J; Hung, A. M; and Edwards, T. L\n\n\n \n \n \n \n Trans-ethnic association study of blood pressure determinants in over 750,000 individuals.\n \n \n \n\n\n \n\n\n\n Nat Genet, 51: 51–62. January 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{giri_trans-ethnic_2019,\n\ttitle = {Trans-ethnic association study of blood pressure determinants in over 750,000 individuals.},\n\tvolume = {51},\n\tissn = {1546-1718},\n\tdoi = {10.1038/s41588-018-0303-9},\n\tabstract = {{\\textless}p{\\textgreater}In this trans-ethnic multi-omic study, we reinterpret the genetic architecture of blood pressure to identify genes, tissues, phenomes and medication contexts of blood pressure homeostasis. We discovered 208 novel common blood pressure SNPs and 53 rare variants in genome-wide association studies of systolic, diastolic and pulse pressure in up to 776,078 participants from the Million Veteran Program (MVP) and collaborating studies, with analysis of the blood pressure clinical phenome in MVP. Our transcriptome-wide association study detected 4,043 blood pressure associations with genetically predicted gene expression of 840 genes in 45 tissues, and mouse renal single-cell RNA sequencing identified upregulated blood pressure genes in kidney tubule cells.{\\textless}/p{\\textgreater}},\n\tjournal = {Nat Genet},\n\tauthor = {Giri, Ayush and Hellwege, Jacklyn N and Keaton, Jacob M and Park, Jihwan and Qiu, Chengxiang and Warren, Helen R and Torstenson, Eric S and Kovesdy, Csaba P and Sun, Yan V and Wilson, Otis D and Robinson-Cohen, Cassianne and Roumie, Christianne L and Chung, Cecilia P and Birdwell, Kelly A and Damrauer, Scott M and DuVall, Scott L and Klarin, Derek and Cho, Kelly and Wang, Yu and Evangelou, Evangelos and Cabrera, Claudia P and Wain, Louise V and Shrestha, Rojesh and Mautz, Brian S and Akwo, Elvis A and Sargurupremraj, Muralidharan and Debette, Stephanie and Boehnke, Michael and Scott, Laura J and Luan, Jian’an and Zhao, Jing-Hua and Willems, Sara M and Thériault, Sébastien and Shah, Nabi and Oldmeadow, Christopher and Almgren, Peter and Li-Gao, Ruifang and Verweij, Niek and Boutin, Thibaud S and Mangino, Massimo and Ntalla, Ioanna and Feofanova, Elena and Surendran, Praveen and Cook, James P and Karthikeyan, Savita and Lahrouchi, Najim and Liu, Chunyu and Sepúlveda, Nuno and Richardson, Tom G and Kraja, Aldi and Amouyel, Philippe and Farrall, Martin and Poulter, Neil R and Laakso, Markku and Zeggini, Eleftheria and Sever, Peter and Scott, Robert A and Langenberg, Claudia and Wareham, Nicholas J and Conen, David and Palmer, Colin Neil Alexander and Attia, John and Chasman, Daniel I and Ridker, Paul M and Melander, Olle and Mook-Kanamori, Dennis Owen and Harst, Pim van der and Cucca, Francesco and Schlessinger, David and Hayward, Caroline and Spector, Tim D and Jarvelin, Marjo-Riitta and Hennig, Branwen J and Timpson, Nicholas J and Wei, Wei-Qi and Smith, Joshua C and Xu, Yaomin and Matheny, Michael E and Siew, Edward E and Lindgren, Cecilia and Herzig, Karl-Heinz and Dedoussis, George and Denny, Joshua C and Psaty, Bruce M and Howson, Joanna M M and Munroe, Patricia B and Newton-Cheh, Christopher and Caulfield, Mark J and Elliott, Paul and Gaziano, J Michael and Concato, John and Wilson, Peter W F and Tsao, Philip S and Velez Edwards, Digna R and Susztak, Katalin and O’Donnell, Christopher J and Hung, Adriana M and Edwards, Todd L},\n\tmonth = jan,\n\tyear = {2019},\n\tpages = {51--62},\n}\n\n\n\n

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\n \n\n \n \n Tin, A.; Marten, J.; Halperin Kuhns, V. L; Li, Y.; Wuttke, M.; Kirsten, H.; Sieber, K. B; Qiu, C.; Gorski, M.; Yu, Z.; Giri, A.; Sveinbjornsson, G.; Li, M.; Chu, A. Y; Hoppmann, A.; O’Connor, L. J; Prins, B.; Nutile, T.; Noce, D.; Akiyama, M.; Cocca, M.; Ghasemi, S.; van der Most, P. J; Horn, K.; Xu, Y.; Fuchsberger, C.; Sedaghat, S.; Afaq, S.; Amin, N.; Arnlöv, J.; Bakker, S. J L; Bansal, N.; Baptista, D.; Bergmann, S.; Biggs, M. L; Biino, G.; Boerwinkle, E.; Bottinger, E. P; Boutin, T. S; Brumat, M.; Burkhardt, R.; Campana, E.; Campbell, A.; Campbell, H.; Carroll, R. J; Catamo, E.; Chambers, J. C; Ciullo, M.; Concas, M. P.; Coresh, J.; Corre, T.; Cusi, D.; Felicita, S. C.; de Borst, M. H; De Grandi, A.; de Mutsert, R.; de Vries, A. P J; Delgado, G.; Demirkan, A.; Devuyst, O.; Dittrich, K.; Eckardt, K.; Ehret, G.; Endlich, K.; Evans, M. K; Gansevoort, R. T; Gasparini, P.; Giedraitis, V.; Gieger, C.; Girotto, G.; Gögele, M.; Gordon, S. D; Gudbjartsson, D. F; Gudnason, V.; Haller, T.; Hamet, P.; Harris, T. B; Hayward, C.; Hicks, A. A; Hofer, E.; Holm, H.; Huang, W.; Hutri-Kähönen, N.; Hwang, S.; Ikram, M A.; Lewis, R. M; Ingelsson, E.; Jakobsdottir, J.; Jonsdottir, I.; Jonsson, H.; Joshi, P. K; Josyula, N. S.; Jung, B.; Kähönen, M.; Kamatani, Y.; Kanai, M.; Kerr, S. M; Kiess, W.; Kleber, M. E; Koenig, W.; Kooner, J. S; Körner, A.; Kovacs, P.; Krämer, B. K; Kronenberg, F.; Kubo, M.; Kuhnel, B.; La Bianca, M.; Lange, L. A; Lehne, B.; Lehtimäki, T.; Liu, J.; Loeffler, M.; Loos, R. J F; Lyytikäinen, L.; Mägi, R.; Mahajan, A.; Martin, N. G; März, W.; Mascalzoni, D.; Matsuda, K.; Meisinger, C.; Meitinger, T.; Metspalu, A.; Milaneschi, Y.; O’Donnell, C. J; Wilson, O. D; Gaziano, J M.; Mishra, P. P; Mohlke, K. L; Mononen, N.; Montgomery, G. W; Mook-Kanamori, D. O; Müller-Nurasyid, M.; Nadkarni, G. N; Nalls, M. A; Nauck, M.; Nikus, K.; Ning, B.; Nolte, I. M; Noordam, R.; O’Connell, J. R; Olafsson, I.; Padmanabhan, S.; Penninx, B. W J H; Perls, T.; Peters, A.; Pirastu, M.; Pirastu, N.; Pistis, G.; Polasek, O.; Ponte, B.; Porteous, D. J; Poulain, T.; Preuss, M. H; Rabelink, T. J; Raffield, L. M; Raitakari, O. T; Rettig, R.; Rheinberger, M.; Rice, K. M; Rizzi, F.; Robino, A.; Rudan, I.; Krajcoviechova, A.; Cifkova, R.; Rueedi, R.; Ruggiero, D.; Ryan, K. A; Saba, Y.; Salvi, E.; Schmidt, H.; Schmidt, R.; Shaffer, C. M; Smith, A. V; Smith, B. H; Spracklen, C. N; Strauch, K.; Stumvoll, M.; Sulem, P.; Tajuddin, S. M; Teren, A.; Thiery, J.; Thio, C. H L; Thorsteinsdottir, U.; Toniolo, D.; Tönjes, A.; Tremblay, J.; Uitterlinden, A. G; Vaccargiu, S.; van der Harst, P.; van Duijn, C. M; Verweij, N.; Völker, U.; Vollenweider, P.; Waeber, G.; Waldenberger, M.; Whitfield, J. B; Wild, S. H; Wilson, J. F; Yang, Q.; Zhang, W.; Zonderman, A. B; Bochud, M.; Wilson, J. G; Pendergrass, S. A; Ho, K.; Parsa, A.; Pramstaller, P. P; Psaty, B. M; Böger, C. A; Snieder, H.; Butterworth, A. S; Okada, Y.; Edwards, T. L; Stefansson, K.; Susztak, K.; Scholz, M.; Heid, I. M; Hung, A. M; Teumer, A.; Pattaro, C.; Woodward, O. M; Vitart, V.; and Köttgen, A.\n\n\n \n \n \n \n Target genes, variants, tissues and transcriptional pathways influencing human serum urate levels.\n \n \n \n\n\n \n\n\n\n Nat Genet, 51: 1459–1474. October 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{tin_target_2019,\n\ttitle = {Target genes, variants, tissues and transcriptional pathways influencing human serum urate levels.},\n\tvolume = {51},\n\tissn = {1546-1718},\n\tdoi = {10.1038/s41588-019-0504-x},\n\tabstract = {{\\textless}p{\\textgreater}Elevated serum urate levels cause gout and correlate with cardiometabolic diseases via poorly understood mechanisms. We performed a trans-ancestry genome-wide association study of serum urate in 457,690 individuals, identifying 183 loci (147 previously unknown) that improve the prediction of gout in an independent cohort of 334,880 individuals. Serum urate showed significant genetic correlations with many cardiometabolic traits, with genetic causality analyses supporting a substantial role for pleiotropy. Enrichment analysis, fine-mapping of urate-associated loci and colocalization with gene expression in 47 tissues implicated the kidney and liver as the main target organs and prioritized potentially causal genes and variants, including the transcriptional master regulators in the liver and kidney, HNF1A and HNF4A. Experimental validation showed that HNF4A transactivated the promoter of ABCG2, encoding a major urate transporter, in kidney cells, and that HNF4A p.Thr139Ile is a functional variant. Transcriptional coregulation within and across organs may be a general mechanism underlying the observed pleiotropy between urate and cardiometabolic traits.{\\textless}/p{\\textgreater}},\n\tjournal = {Nat Genet},\n\tauthor = {Tin, Adrienne and Marten, Jonathan and Halperin Kuhns, Victoria L and Li, Yong and Wuttke, Matthias and Kirsten, Holger and Sieber, Karsten B and Qiu, Chengxiang and Gorski, Mathias and Yu, Zhi and Giri, Ayush and Sveinbjornsson, Gardar and Li, Man and Chu, Audrey Y and Hoppmann, Anselm and O’Connor, Luke J and Prins, Bram and Nutile, Teresa and Noce, Damia and Akiyama, Masato and Cocca, Massimiliano and Ghasemi, Sahar and van der Most, Peter J and Horn, Katrin and Xu, Yizhe and Fuchsberger, Christian and Sedaghat, Sanaz and Afaq, Saima and Amin, Najaf and Arnlöv, Johan and Bakker, Stephan J L and Bansal, Nisha and Baptista, Daniela and Bergmann, Sven and Biggs, Mary L and Biino, Ginevra and Boerwinkle, Eric and Bottinger, Erwin P and Boutin, Thibaud S and Brumat, Marco and Burkhardt, Ralph and Campana, Eric and Campbell, Archie and Campbell, Harry and Carroll, Robert J and Catamo, Eulalia and Chambers, John C and Ciullo, Marina and Concas, Maria Pina and Coresh, Josef and Corre, Tanguy and Cusi, Daniele and Felicita, Sala Cinzia and de Borst, Martin H and De Grandi, Alessandro and de Mutsert, Renée and de Vries, Aiko P J and Delgado, Graciela and Demirkan, Ayse and Devuyst, Olivier and Dittrich, Katalin and Eckardt, Kai-Uwe and Ehret, Georg and Endlich, Karlhans and Evans, Michele K and Gansevoort, Ron T and Gasparini, Paolo and Giedraitis, Vilmantas and Gieger, Christian and Girotto, Giorgia and Gögele, Martin and Gordon, Scott D and Gudbjartsson, Daniel F and Gudnason, Vilmundur and Haller, Toomas and Hamet, Pavel and Harris, Tamara B and Hayward, Caroline and Hicks, Andrew A and Hofer, Edith and Holm, Hilma and Huang, Wei and Hutri-Kähönen, Nina and Hwang, Shih-Jen and Ikram, M Arfan and Lewis, Raychel M and Ingelsson, Erik and Jakobsdottir, Johanna and Jonsdottir, Ingileif and Jonsson, Helgi and Joshi, Peter K and Josyula, Navya Shilpa and Jung, Bettina and Kähönen, Mika and Kamatani, Yoichiro and Kanai, Masahiro and Kerr, Shona M and Kiess, Wieland and Kleber, Marcus E and Koenig, Wolfgang and Kooner, Jaspal S and Körner, Antje and Kovacs, Peter and Krämer, Bernhard K and Kronenberg, Florian and Kubo, Michiaki and Kuhnel, Brigitte and La Bianca, Martina and Lange, Leslie A and Lehne, Benjamin and Lehtimäki, Terho and Liu, Jun and Loeffler, Markus and Loos, Ruth J F and Lyytikäinen, Leo-Pekka and Mägi, Reedik and Mahajan, Anubha and Martin, Nicholas G and März, Winfried and Mascalzoni, Deborah and Matsuda, Koichi and Meisinger, Christa and Meitinger, Thomas and Metspalu, Andres and Milaneschi, Yuri and O’Donnell, Christopher J and Wilson, Otis D and Gaziano, J Michael and Mishra, Pashupati P and Mohlke, Karen L and Mononen, Nina and Montgomery, Grant W and Mook-Kanamori, Dennis O and Müller-Nurasyid, Martina and Nadkarni, Girish N and Nalls, Mike A and Nauck, Matthias and Nikus, Kjell and Ning, Boting and Nolte, Ilja M and Noordam, Raymond and O’Connell, Jeffrey R and Olafsson, Isleifur and Padmanabhan, Sandosh and Penninx, Brenda W J H and Perls, Thomas and Peters, Annette and Pirastu, Mario and Pirastu, Nicola and Pistis, Giorgio and Polasek, Ozren and Ponte, Belen and Porteous, David J and Poulain, Tanja and Preuss, Michael H and Rabelink, Ton J and Raffield, Laura M and Raitakari, Olli T and Rettig, Rainer and Rheinberger, Myriam and Rice, Kenneth M and Rizzi, Federica and Robino, Antonietta and Rudan, Igor and Krajcoviechova, Alena and Cifkova, Renata and Rueedi, Rico and Ruggiero, Daniela and Ryan, Kathleen A and Saba, Yasaman and Salvi, Erika and Schmidt, Helena and Schmidt, Reinhold and Shaffer, Christian M and Smith, Albert V and Smith, Blair H and Spracklen, Cassandra N and Strauch, Konstantin and Stumvoll, Michael and Sulem, Patrick and Tajuddin, Salman M and Teren, Andrej and Thiery, Joachim and Thio, Chris H L and Thorsteinsdottir, Unnur and Toniolo, Daniela and Tönjes, Anke and Tremblay, Johanne and Uitterlinden, André G and Vaccargiu, Simona and van der Harst, Pim and van Duijn, Cornelia M and Verweij, Niek and Völker, Uwe and Vollenweider, Peter and Waeber, Gérard and Waldenberger, Melanie and Whitfield, John B and Wild, Sarah H and Wilson, James F and Yang, Qiong and Zhang, Weihua and Zonderman, Alan B and Bochud, Murielle and Wilson, James G and Pendergrass, Sarah A and Ho, Kevin and Parsa, Afshin and Pramstaller, Peter P and Psaty, Bruce M and Böger, Carsten A and Snieder, Harold and Butterworth, Adam S and Okada, Yukinori and Edwards, Todd L and Stefansson, Kari and Susztak, Katalin and Scholz, Markus and Heid, Iris M and Hung, Adriana M and Teumer, Alexander and Pattaro, Cristian and Woodward, Owen M and Vitart, Veronique and Köttgen, Anna},\n\tmonth = oct,\n\tyear = {2019},\n\tpages = {1459--1474},\n}\n\n\n\n

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\n \n\n \n \n Ebbert, M. T W; Jensen, T. D; Jansen-West, K.; Sens, J. P; Reddy, J. S; Ridge, P. G; Kauwe, J. S K; Belzil, V.; Pregent, L.; Carrasquillo, M. M; Keene, D.; Larson, E.; Crane, P.; Asmann, Y. W; Ertekin-Taner, N.; Younkin, S. G; Ross, O. A; Rademakers, R.; Petrucelli, L.; and Fryer, J. D\n\n\n \n \n \n \n Systematic analysis of dark and camouflaged genes reveals disease-relevant genes hiding in plain sight.\n \n \n \n\n\n \n\n\n\n Genome Biol, 20: 97. 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{ebbert_systematic_2019,\n\ttitle = {Systematic analysis of dark and camouflaged genes reveals disease-relevant genes hiding in plain sight.},\n\tvolume = {20},\n\tissn = {1474-760X},\n\tdoi = {10.1186/s13059-019-1707-2},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{BACKGROUND: }The human genome contains "dark" gene regions that cannot be adequately assembled or aligned using standard short-read sequencing technologies, preventing researchers from identifying mutations within these gene regions that may be relevant to human disease. Here, we identify regions with few mappable reads that we call dark by depth, and others that have ambiguous alignment, called camouflaged. We assess how well long-read or linked-read technologies resolve these regions.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{RESULTS: }Based on standard whole-genome Illumina sequencing data, we identify 36,794 dark regions in 6054 gene bodies from pathways important to human health, development, and reproduction. Of these gene bodies, 8.7\\% are completely dark and 35.2\\% are {\\textgreater}= 5\\% dark. We identify dark regions that are present in protein-coding exons across 748 genes. Linked-read or long-read sequencing technologies from 10x Genomics, PacBio, and Oxford Nanopore Technologies reduce dark protein-coding regions to approximately 50.5\\%, 35.6\\%, and 9.6\\%, respectively. We present an algorithm to resolve most camouflaged regions and apply it to the Alzheimer’s Disease Sequencing Project. We rescue a rare ten-nucleotide frameshift deletion in CR1, a top Alzheimer’s disease gene, found in disease cases but not in controls.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSIONS: }While we could not formally assess the association of the CR1 frameshift mutation with Alzheimer’s disease due to insufficient sample-size, we believe it merits investigating in a larger cohort. There remain thousands of potentially important genomic regions overlooked by short-read sequencing that are largely resolved by long-read technologies.{\\textless}/p{\\textgreater}},\n\tjournal = {Genome Biol},\n\tauthor = {Ebbert, Mark T W and Jensen, Tanner D and Jansen-West, Karen and Sens, Jonathon P and Reddy, Joseph S and Ridge, Perry G and Kauwe, John S K and Belzil, Veronique and Pregent, Luc and Carrasquillo, Minerva M and Keene, Dirk and Larson, Eric and Crane, Paul and Asmann, Yan W and Ertekin-Taner, Nilufer and Younkin, Steven G and Ross, Owen A and Rademakers, Rosa and Petrucelli, Leonard and Fryer, John D},\n\tyear = {2019},\n\tkeywords = {Genetic Predisposition to Disease, Genome, Human, Humans, Mutation},\n\tpages = {97},\n}\n\n\n\n

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\n \n\n \n \n Larsson, S. C; Traylor, M.; Burgess, S.; Boncoraglio, G. B; Jern, C.; Michaëlsson, K.; and Markus, H. S\n\n\n \n \n \n \n Serum magnesium and calcium levels in relation to ischemic stroke: Mendelian randomization study.\n \n \n \n\n\n \n\n\n\n Neurology, 92: e944–e950. February 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{larsson_serum_2019,\n\ttitle = {Serum magnesium and calcium levels in relation to ischemic stroke: {Mendelian} randomization study.},\n\tvolume = {92},\n\tissn = {1526-632X},\n\tdoi = {10.1212/WNL.0000000000007001},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{OBJECTIVE: }To determine whether serum magnesium and calcium concentrations are causally associated with ischemic stroke or any of its subtypes using the mendelian randomization approach.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS: }Analyses were conducted using summary statistics data for 13 single-nucleotide polymorphisms robustly associated with serum magnesium (n = 6) or serum calcium (n = 7) concentrations. The corresponding data for ischemic stroke were obtained from the MEGASTROKE consortium (34,217 cases and 404,630 noncases).{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{RESULTS: }In standard mendelian randomization analysis, the odds ratios for each 0.1 mmol/L (about 1 SD) increase in genetically predicted serum magnesium concentrations were 0.78 (95\\% confidence interval [CI] 0.69-0.89; = 1.3 × 10) for all ischemic stroke, 0.63 (95\\% CI 0.50-0.80; = 1.6 × 10) for cardioembolic stroke, and 0.60 (95\\% CI 0.44-0.82; = 0.001) for large artery stroke; there was no association with small vessel stroke (odds ratio 0.90, 95\\% CI 0.67-1.20; = 0.46). Only the association with cardioembolic stroke was robust in sensitivity analyses. There was no association of genetically predicted serum calcium concentrations with all ischemic stroke (per 0.5 mg/dL [about 1 SD] increase in serum calcium: odds ratio 1.03, 95\\% CI 0.88-1.21) or with any subtype.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSIONS: }This study found that genetically higher serum magnesium concentrations are associated with a reduced risk of cardioembolic stroke but found no significant association of genetically higher serum calcium concentrations with any ischemic stroke subtype.{\\textless}/p{\\textgreater}},\n\tjournal = {Neurology},\n\tauthor = {Larsson, Susanna C and Traylor, Matthew and Burgess, Stephen and Boncoraglio, Giorgio B and Jern, Christina and Michaëlsson, Karl and Markus, Hugh S},\n\tmonth = feb,\n\tyear = {2019},\n\tpages = {e944--e950},\n}\n\n\n\n

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\n \n\n \n \n Miller, L. M; Peralta, C. A; Fitzpatrick, A. L; Wu, C.; Psaty, B. M; Newman, A. B; and Odden, M. C\n\n\n \n \n \n \n The role of functional status on the relationship between blood pressure and cognitive decline: the Cardiovascular Health Study.\n \n \n \n\n\n \n\n\n\n J Hypertens. May 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{miller_role_2019,\n\ttitle = {The role of functional status on the relationship between blood pressure and cognitive decline: the {Cardiovascular} {Health} {Study}.},\n\tissn = {1473-5598},\n\tdoi = {10.1097/HJH.0000000000002102},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{OBJECTIVE: }To examine whether self-reported functional status modified the association between blood pressure (BP) and cognitive decline among older adults.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS: }The study included 2097 US adults aged 75 years and older from the Cardiovascular Health Study, followed for up to 6 years. Functional status was ascertained by self-reported limitation in activities of daily living (ADL; none vs. any). Cognitive function was assessed by the Modified Mini Mental State Exam (3MSE). We used linear mixed models to examine whether the presence of at least one ADL limitation modified the association between BP and cognitive decline. Potential confounders included demographics, physiologic measures, antihypertensive medication use and apolipoprotein E ε4 allele. We conducted stratified analyses for significant interactions between BP and ADL.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{RESULTS: }The association between BP and change in 3MSE differed by baseline ADL limitation. Among participants without ADL limitation, elevated systolic BP ({\\textgreater}=140 mmHg) was associated with a 0.15 decrease (95\\% CI -0.24 to -0.07); P value for interaction less than 0.001, whereas in those with an ADL limitation, elevated systolic BP was independently associated with a 0.30 increase in 3MSE scores per year (95\\% CI 0.06-0.55). Elevated diastolic BP ({\\textgreater}=80 mmHg) was associated with an increase in cognitive function in both groups, although the increase was greater in those with ADL limitation (0.47 points per year vs. 0.18 points per year, P value for interaction = 0.01).{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSION: }Elevated BP appears to be associated with a decrease in cognitive scores among functioning older adults, and modest improvements in cognitive function among poorly functioning elders.{\\textless}/p{\\textgreater}},\n\tjournal = {J Hypertens},\n\tauthor = {Miller, Lindsay M and Peralta, Carmen A and Fitzpatrick, Annette L and Wu, Chenkai and Psaty, Bruce M and Newman, Anne B and Odden, Michelle C},\n\tmonth = may,\n\tyear = {2019},\n}\n\n\n\n

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\n \n\n \n \n Zhang, X.; Zhu, C.; Beecham, G.; Vardarajan, B. N; Ma, Y.; Lancour, D.; Farrell, J. J; Chung, J.; Mayeux, R.; Haines, J. L; Schellenberg, G. D; Pericak-Vance, M. A; Lunetta, K. L; and Farrer, L. A\n\n\n \n \n \n \n A rare missense variant of CASP7 is associated with familial late-onset Alzheimer’s disease.\n \n \n \n\n\n \n\n\n\n Alzheimers Dement. January 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{zhang_rare_2019,\n\ttitle = {A rare missense variant of {CASP7} is associated with familial late-onset {Alzheimer}’s disease.},\n\tissn = {1552-5279},\n\tdoi = {10.1016/j.jalz.2018.10.005},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{INTRODUCTION: }The genetic architecture of Alzheimer’s disease (AD) is only partially understood.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS: }We conducted an association study for AD using whole sequence data from 507 genetically enriched AD cases (i.e., cases having close relatives affected by AD) and 4917 cognitively healthy controls of European ancestry (EA) and 172 enriched cases and 179 controls of Caribbean Hispanic ancestry. Confirmation of top findings from stage 1 was sought in two family-based genome-wide association study data sets and in a whole genome-sequencing data set comprising members from 42 EA and 115 Caribbean Hispanic families.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{RESULTS: }We identified associations in EAs with variants in 12 novel loci. The most robust finding is a rare CASP7 missense variant (rs116437863; P = 2.44 × 10) which improved when combined with results from stage 2 data sets (P = 1.92 × 10).{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{DISCUSSION: }Our study demonstrated that an enriched case design can strengthen genetic signals, thus allowing detection of associations that would otherwise be missed in a traditional case-control study.{\\textless}/p{\\textgreater}},\n\tjournal = {Alzheimers Dement},\n\tauthor = {Zhang, Xiaoling and Zhu, Congcong and Beecham, Gary and Vardarajan, Badri N and Ma, Yiyi and Lancour, Daniel and Farrell, John J and Chung, Jaeyoon and Mayeux, Richard and Haines, Jonathan L and Schellenberg, Gerard D and Pericak-Vance, Margaret A and Lunetta, Kathryn L and Farrer, Lindsay A},\n\tmonth = jan,\n\tyear = {2019},\n}\n\n\n\n

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\n \n\n \n \n Liang, J.; Cade, B. E; He, K. Y; Wang, H.; Lee, J.; Sofer, T.; Williams, S.; Li, R.; Chen, H.; Gottlieb, D. J; Evans, D. S; Guo, X.; Gharib, S. A; Hale, L.; Hillman, D. R; Lutsey, P. L; Mukherjee, S.; Ochs-Balcom, H. M; Palmer, L. J; Rhodes, J.; Purcell, S.; Patel, S. R; Saxena, R.; Stone, K. L; Tang, W.; Tranah, G. J; Boerwinkle, E.; Lin, X.; Liu, Y.; Psaty, B. M; Vasan, R. S; Cho, M. H; Manichaikul, A.; Silverman, E. K; Barr, R G.; Rich, S. S; Rotter, J. I; Wilson, J. G; Redline, S.; and Zhu, X.\n\n\n \n \n \n \n Sequencing Analysis at 8p23 Identifies Multiple Rare Variants in DLC1 Associated with Sleep-Related Oxyhemoglobin Saturation Level.\n \n \n \n\n\n \n\n\n\n Am J Hum Genet, 105: 1057–1068. November 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{liang_sequencing_2019,\n\ttitle = {Sequencing {Analysis} at 8p23 {Identifies} {Multiple} {Rare} {Variants} in {DLC1} {Associated} with {Sleep}-{Related} {Oxyhemoglobin} {Saturation} {Level}.},\n\tvolume = {105},\n\tissn = {1537-6605},\n\tdoi = {10.1016/j.ajhg.2019.10.002},\n\tabstract = {{\\textless}p{\\textgreater}Average arterial oxyhemoglobin saturation during sleep (AvSpOS) is a clinically relevant measure of physiological stress associated with sleep-disordered breathing, and this measure predicts incident cardiovascular disease and mortality. Using high-depth whole-genome sequencing data from the National Heart, Lung, and Blood Institute (NHLBI) Trans-Omics for Precision Medicine (TOPMed) project and focusing on genes with linkage evidence on chromosome 8p23, we observed that six coding and 51 noncoding variants in a gene that encodes the GTPase-activating protein (DLC1) are significantly associated with AvSpOS and replicated in independent subjects. The combined DLC1 association evidence of discovery and replication cohorts reaches genome-wide significance in European Americans (p = 7.9 × 10). A risk score for these variants, built on an independent dataset, explains 0.97\\% of the AvSpOS variation and contributes to the linkage evidence. The 51 noncoding variants are enriched in regulatory features in a human lung fibroblast cell line and contribute to DLC1 expression variation. Mendelian randomization analysis using these variants indicates a significant causal effect of DLC1 expression in fibroblasts on AvSpOS. Multiple sources of information, including genetic variants, gene expression, and methylation, consistently suggest that DLC1 is a gene associated with AvSpOS.{\\textless}/p{\\textgreater}},\n\tjournal = {Am J Hum Genet},\n\tauthor = {Liang, Jingjing and Cade, Brian E and He, Karen Y and Wang, Heming and Lee, Jiwon and Sofer, Tamar and Williams, Stephanie and Li, Ruitong and Chen, Han and Gottlieb, Daniel J and Evans, Daniel S and Guo, Xiuqing and Gharib, Sina A and Hale, Lauren and Hillman, David R and Lutsey, Pamela L and Mukherjee, Sutapa and Ochs-Balcom, Heather M and Palmer, Lyle J and Rhodes, Jessica and Purcell, Shaun and Patel, Sanjay R and Saxena, Richa and Stone, Katie L and Tang, Weihong and Tranah, Gregory J and Boerwinkle, Eric and Lin, Xihong and Liu, Yongmei and Psaty, Bruce M and Vasan, Ramachandran S and Cho, Michael H and Manichaikul, Ani and Silverman, Edwin K and Barr, R Graham and Rich, Stephen S and Rotter, Jerome I and Wilson, James G and Redline, Susan and Zhu, Xiaofeng},\n\tmonth = nov,\n\tyear = {2019},\n\tpages = {1057--1068},\n}\n\n\n\n

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\n \n\n \n \n O’Rourke, M. F; and Adji, A.\n\n\n \n \n \n \n The role of functional status on the relationship between blood pressure and cognitive decline: the Cardiovascular Health Study.\n \n \n \n\n\n \n\n\n\n J Hypertens, 37: 2500–2501. December 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{orourke_role_2019,\n\ttitle = {The role of functional status on the relationship between blood pressure and cognitive decline: the {Cardiovascular} {Health} {Study}.},\n\tvolume = {37},\n\tissn = {1473-5598},\n\tdoi = {10.1097/HJH.0000000000002263},\n\tjournal = {J Hypertens},\n\tauthor = {O’Rourke, Michael F and Adji, Audrey},\n\tmonth = dec,\n\tyear = {2019},\n\tpages = {2500--2501},\n}\n\n\n\n

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\n \n\n \n \n Fleck, D.; Phu, L.; Verschueren, E.; Hinkle, T.; Reichelt, M.; Bhangale, T.; Haley, B.; Wang, Y.; Graham, R.; Kirkpatrick, D. S; Sheng, M.; and Bingol, B.\n\n\n \n \n \n \n PTCD1 Is Required for Mitochondrial Oxidative-Phosphorylation: Possible Genetic Association with Alzheimer’s Disease.\n \n \n \n\n\n \n\n\n\n J Neurosci, 39: 4636–4656. June 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{fleck_ptcd1_2019,\n\ttitle = {{PTCD1} {Is} {Required} for {Mitochondrial} {Oxidative}-{Phosphorylation}: {Possible} {Genetic} {Association} with {Alzheimer}’s {Disease}.},\n\tvolume = {39},\n\tissn = {1529-2401},\n\tdoi = {10.1523/JNEUROSCI.0116-19.2019},\n\tabstract = {{\\textless}p{\\textgreater}In addition to amyloid-β plaques and tau tangles, mitochondrial dysfunction is implicated in the pathology of Alzheimer’s disease (AD). Neurons heavily rely on mitochondrial function, and deficits in brain energy metabolism are detected early in AD; however, direct human genetic evidence for mitochondrial involvement in AD pathogenesis is limited. We analyzed whole-exome sequencing data of 4549 AD cases and 3332 age-matched controls and discovered that rare protein altering variants in the gene pentatricopeptide repeat-containing protein 1 () show a trend for enrichment in cases compared with controls. We show here that PTCD1 is required for normal mitochondrial rRNA levels, proper assembly of the mitochondrial ribosome and hence for mitochondrial translation and assembly of the electron transport chain. Loss of PTCD1 function impairs oxidative phosphorylation and forces cells to rely on glycolysis for energy production. Cells expressing the AD-linked variant of PTCD1 fail to sustain energy production under increased metabolic stress. In neurons, reduced PTCD1 expression leads to lower ATP levels and impacts spontaneous synaptic activity. Thus, our study uncovers a possible link between a protein required for mitochondrial function and energy metabolism and AD risk. Mitochondria are the main source of cellular energy and mitochondrial dysfunction is implicated in the pathology of Alzheimer’s disease (AD) and other neurodegenerative disorders. Here, we identify a variant in the gene that is enriched in AD patients and demonstrate that PTCD1 is required for ATP generation through oxidative phosphorylation. PTCD1 regulates the level of 16S rRNA, the backbone of the mitoribosome, and is essential for mitochondrial translation and assembly of the electron transport chain. Cells expressing the AD-associated variant fail to maintain adequate ATP production during metabolic stress, and reduced PTCD1 activity disrupts neuronal energy homeostasis and dampens spontaneous transmission. Our work provides a mechanistic link between a protein required for mitochondrial function and genetic AD risk.{\\textless}/p{\\textgreater}},\n\tjournal = {J Neurosci},\n\tauthor = {Fleck, Daniel and Phu, Lilian and Verschueren, Erik and Hinkle, Trent and Reichelt, Mike and Bhangale, Tushar and Haley, Benjamin and Wang, Yuanyuan and Graham, Robert and Kirkpatrick, Donald S and Sheng, Morgan and Bingol, Baris},\n\tmonth = jun,\n\tyear = {2019},\n\tpages = {4636--4656},\n}\n\n\n\n

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\n \\textlessp\\textgreaterIn addition to amyloid-β plaques and tau tangles, mitochondrial dysfunction is implicated in the pathology of Alzheimer’s disease (AD). Neurons heavily rely on mitochondrial function, and deficits in brain energy metabolism are detected early in AD; however, direct human genetic evidence for mitochondrial involvement in AD pathogenesis is limited. We analyzed whole-exome sequencing data of 4549 AD cases and 3332 age-matched controls and discovered that rare protein altering variants in the gene pentatricopeptide repeat-containing protein 1 () show a trend for enrichment in cases compared with controls. We show here that PTCD1 is required for normal mitochondrial rRNA levels, proper assembly of the mitochondrial ribosome and hence for mitochondrial translation and assembly of the electron transport chain. Loss of PTCD1 function impairs oxidative phosphorylation and forces cells to rely on glycolysis for energy production. Cells expressing the AD-linked variant of PTCD1 fail to sustain energy production under increased metabolic stress. In neurons, reduced PTCD1 expression leads to lower ATP levels and impacts spontaneous synaptic activity. Thus, our study uncovers a possible link between a protein required for mitochondrial function and energy metabolism and AD risk. Mitochondria are the main source of cellular energy and mitochondrial dysfunction is implicated in the pathology of Alzheimer’s disease (AD) and other neurodegenerative disorders. Here, we identify a variant in the gene that is enriched in AD patients and demonstrate that PTCD1 is required for ATP generation through oxidative phosphorylation. PTCD1 regulates the level of 16S rRNA, the backbone of the mitoribosome, and is essential for mitochondrial translation and assembly of the electron transport chain. Cells expressing the AD-associated variant fail to maintain adequate ATP production during metabolic stress, and reduced PTCD1 activity disrupts neuronal energy homeostasis and dampens spontaneous transmission. Our work provides a mechanistic link between a protein required for mitochondrial function and genetic AD risk.\\textless/p\\textgreater\n

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\n \n\n \n \n Lemaitre, R. N; Jensen, P. N; Hoofnagle, A.; McKnight, B.; Fretts, A. M; King, I. B; Siscovick, D. S; Psaty, B. M; Heckbert, S. R; Mozaffarian, D.; and Sotoodehnia, N.\n\n\n \n \n \n \n Plasma Ceramides and Sphingomyelins in Relation to Heart Failure Risk.\n \n \n \n\n\n \n\n\n\n Circ Heart Fail, 12: e005708. July 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{lemaitre_plasma_2019,\n\ttitle = {Plasma {Ceramides} and {Sphingomyelins} in {Relation} to {Heart} {Failure} {Risk}.},\n\tvolume = {12},\n\tissn = {1941-3297},\n\tdoi = {10.1161/CIRCHEARTFAILURE.118.005708},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{BACKGROUND: }Ceramides exhibit multiple biological activities that may influence the pathophysiology of heart failure. These activities may be influenced by the saturated fatty acid carried by the ceramide (Cer). However, the associations of different circulating Cer species, and their sphingomyelin (SM) precursors, with heart failure have received limited attention.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS AND RESULTS: }We studied the associations of plasma Cer and SM species with incident heart failure in the Cardiovascular Health Study. We examined 8 species: Cer and SM with palmitic acid (Cer-16 and SM-16), species with arachidic acid (Cer-20 and SM-20), species with behenic acid (Cer-22 and SM-22), and species with lignoceric acid (Cer-24 and SM-24). During a median follow-up of 9.4 years, we identified 1179 cases of incident heart failure among 4249 study participants. In Cox regression analyses adjusted for risk factors, higher levels of Cer-16 and SM-16 were associated with higher risk of incident heart failure (hazard ratio for one SD increase:1.25 [95\\% CI, 1.16-1.36] and 1.28 [1.18-1.40], respectively). In contrast, higher levels of Cer-22 were associated with lower risk of heart failure in multivariable analyses further adjusted for Cer-16 (hazard ratio, 0.85 [0.78-0.92]); and higher levels of SM-20, SM-22 and SM-24 were associated with lower risk of heart failure in analyses further adjusted for SM-16 (hazard ratios, 0.83 [0.77-0.90], 0.81 [0.75-0.88], and 0.83 [0.77-0.90], respectively). No statistically significant interactions with age, sex, black race, body mass index, or baseline coronary heart disease were detected. Similar associations were observed for heart failure with preserved (n=529) or reduced (n=348) ejection fraction.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSIONS: }This study shows associations of higher plasma levels of Cer-16 and SM-16 with increased risk of heart failure and higher levels of Cer-22, SM-20, SM-22, and SM-24 with decreased risk of heart failure.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CLINICAL TRIAL REGISTRATION: }URL: https://www.clinicaltrials.gov . Unique identifier: NCT00005133.{\\textless}/p{\\textgreater}},\n\tjournal = {Circ Heart Fail},\n\tauthor = {Lemaitre, Rozenn N and Jensen, Paul N and Hoofnagle, Andrew and McKnight, Barbara and Fretts, Amanda M and King, Irena B and Siscovick, David S and Psaty, Bruce M and Heckbert, Susan R and Mozaffarian, Dariush and Sotoodehnia, Nona},\n\tmonth = jul,\n\tyear = {2019},\n\tpages = {e005708},\n}\n\n\n\n

\n\n\n

\n \\textlessp\\textgreater\\textbfBACKGROUND: Ceramides exhibit multiple biological activities that may influence the pathophysiology of heart failure. These activities may be influenced by the saturated fatty acid carried by the ceramide (Cer). However, the associations of different circulating Cer species, and their sphingomyelin (SM) precursors, with heart failure have received limited attention.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfMETHODS AND RESULTS: We studied the associations of plasma Cer and SM species with incident heart failure in the Cardiovascular Health Study. We examined 8 species: Cer and SM with palmitic acid (Cer-16 and SM-16), species with arachidic acid (Cer-20 and SM-20), species with behenic acid (Cer-22 and SM-22), and species with lignoceric acid (Cer-24 and SM-24). During a median follow-up of 9.4 years, we identified 1179 cases of incident heart failure among 4249 study participants. In Cox regression analyses adjusted for risk factors, higher levels of Cer-16 and SM-16 were associated with higher risk of incident heart failure (hazard ratio for one SD increase:1.25 [95% CI, 1.16-1.36] and 1.28 [1.18-1.40], respectively). In contrast, higher levels of Cer-22 were associated with lower risk of heart failure in multivariable analyses further adjusted for Cer-16 (hazard ratio, 0.85 [0.78-0.92]); and higher levels of SM-20, SM-22 and SM-24 were associated with lower risk of heart failure in analyses further adjusted for SM-16 (hazard ratios, 0.83 [0.77-0.90], 0.81 [0.75-0.88], and 0.83 [0.77-0.90], respectively). No statistically significant interactions with age, sex, black race, body mass index, or baseline coronary heart disease were detected. Similar associations were observed for heart failure with preserved (n=529) or reduced (n=348) ejection fraction.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfCONCLUSIONS: This study shows associations of higher plasma levels of Cer-16 and SM-16 with increased risk of heart failure and higher levels of Cer-22, SM-20, SM-22, and SM-24 with decreased risk of heart failure.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfCLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov . Unique identifier: NCT00005133.\\textless/p\\textgreater\n

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\n \n\n \n \n Kerola, T.; Dewland, T. A; Vittinghoff, E.; Heckbert, S. R; Stein, P. K; and Marcus, G. M\n\n\n \n \n \n \n Predictors of atrial ectopy and their relationship to atrial fibrillation risk.\n \n \n \n\n\n \n\n\n\n Europace. March 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{kerola_predictors_2019,\n\ttitle = {Predictors of atrial ectopy and their relationship to atrial fibrillation risk.},\n\tissn = {1532-2092},\n\tdoi = {10.1093/europace/euz008},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{AIMS: }Premature atrial contractions (PACs) are known to trigger and predict atrial fibrillation (AF). We sought to identify the determinants of PACs and the degree to which PACs mediate the effects of established risk factors for AF.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS AND RESULTS: }Predictors of baseline PAC frequency were examined using a Holter Study among 1392 participants in the Cardiovascular Health Study, a community-based cohort of individuals aged {\\textgreater}=65 years. Participants were then followed for their first diagnosis of AF. Independent predictors of PACs were identified, and the extent to which PACs might mediate the relationship between those predictors and AF was determined. The median hourly frequency of PACs was 2.7 (interquartile range 0.8-12.1). After multivariable adjustment, increasing age, increasing height, decreasing body mass index, and a history of myocardial infarction were each associated with more PACs. Regarding modifiable predictors, participants using beta-blockers had 21\\% less [95\\% confidence interval (95\\% CI) 9-30\\%, P = 0.001] and those performing at least moderate intensity exercise vs. lower intensity exercisers had 10\\% less (95\\% CI 1-18\\%, P = 0.03) PACs. Higher PAC frequency explained 34\\% (95\\% CI 22-57\\%, P {\\textless} 0.0001) of the relationship between increasing age and AF risk and 27\\% (95\\% CI 10-75\\%, P = 0.004) of the relationship between taller height and AF risk.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSION: }Enhancing physical activity and use of beta-blockers may represent fruitful strategies to mitigate PAC frequency. A substantial proportion of the excess risk of AF due to increasing age and taller height may be explained by an increase in PAC frequency.{\\textless}/p{\\textgreater}},\n\tjournal = {Europace},\n\tauthor = {Kerola, Tuomas and Dewland, Thomas A and Vittinghoff, Eric and Heckbert, Susan R and Stein, Phyllis K and Marcus, Gregory M},\n\tmonth = mar,\n\tyear = {2019},\n}\n\n\n\n

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\n \n\n \n \n Floyd, J. S; Bloch, K. M; Brody, J. A; Maroteau, C.; Siddiqui, M. K; Gregory, R.; Carr, D. F; Molokhia, M.; Liu, X.; Bis, J. C; Ahmed, A.; Liu, X.; Hallberg, P.; Yue, Q.; Magnusson, P. K E; Brisson, D.; Wiggins, K. L; Morrison, A. C; Khoury, E.; McKeigue, P.; Stricker, B. H; Lapeyre-Mestre, M.; Heckbert, S. R; Gallagher, A. M; Chinoy, H.; Gibbs, R. A; Bondon-Guitton, E.; Tracy, R.; Boerwinkle, E.; Gaudet, D.; Conforti, A.; van Staa, T.; Sitlani, C. M; Rice, K. M; Maitland-van der Zee, A.; Wadelius, M.; Morris, A. P; Pirmohamed, M.; Palmer, C. A N; Psaty, B. M; and Alfirevic, A.\n\n\n \n \n \n \n Pharmacogenomics of statin-related myopathy: Meta-analysis of rare variants from whole-exome sequencing.\n \n \n \n\n\n \n\n\n\n PLoS One, 14: e0218115. 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{floyd_pharmacogenomics_2019,\n\ttitle = {Pharmacogenomics of statin-related myopathy: {Meta}-analysis of rare variants from whole-exome sequencing.},\n\tvolume = {14},\n\tissn = {1932-6203},\n\tdoi = {10.1371/journal.pone.0218115},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{AIMS: }Statin-related myopathy (SRM), which includes rhabdomyolysis, is an uncommon but important adverse drug reaction because the number of people prescribed statins world-wide is large. Previous association studies of common genetic variants have had limited success in identifying a genetic basis for this adverse drug reaction. We conducted a multi-site whole-exome sequencing study to investigate whether rare coding variants confer an increased risk of SRM.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS AND RESULTS: }SRM 3-5 cases (N = 505) and statin treatment-tolerant controls (N = 2047) were recruited from multiple sites in North America and Europe. SRM 3-5 was defined as symptoms consistent with muscle injury and an elevated creatine phosphokinase level {\\textgreater}4 times upper limit of normal without another likely cause of muscle injury. Whole-exome sequencing and variant calling was coordinated from two analysis centres, and results of single-variant and gene-based burden tests were meta-analysed. No genome-wide significant associations were identified. Given the large number of cases, we had 80\\% power to identify a variant with minor allele frequency of 0.01 that increases the risk of SRM 6-fold at genome-wide significance.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSIONS: }In this large whole-exome sequencing study of severe statin-related muscle injury conducted to date, we did not find evidence that rare coding variants are responsible for this adverse drug reaction. Larger sample sizes would be required to identify rare variants with small effects, but it is unclear whether such findings would be clinically actionable.{\\textless}/p{\\textgreater}},\n\tjournal = {PLoS One},\n\tauthor = {Floyd, James S and Bloch, Katarzyna M and Brody, Jennifer A and Maroteau, Cyrielle and Siddiqui, Moneeza K and Gregory, Richard and Carr, Daniel F and Molokhia, Mariam and Liu, Xiaoming and Bis, Joshua C and Ahmed, Ammar and Liu, Xuan and Hallberg, Pär and Yue, Qun-Ying and Magnusson, Patrik K E and Brisson, Diane and Wiggins, Kerri L and Morrison, Alanna C and Khoury, Etienne and McKeigue, Paul and Stricker, Bruno H and Lapeyre-Mestre, Maryse and Heckbert, Susan R and Gallagher, Arlene M and Chinoy, Hector and Gibbs, Richard A and Bondon-Guitton, Emmanuelle and Tracy, Russell and Boerwinkle, Eric and Gaudet, Daniel and Conforti, Anita and van Staa, Tjeerd and Sitlani, Colleen M and Rice, Kenneth M and Maitland-van der Zee, Anke-Hilse and Wadelius, Mia and Morris, Andrew P and Pirmohamed, Munir and Palmer, Colin A N and Psaty, Bruce M and Alfirevic, Ana},\n\tyear = {2019},\n\tpages = {e0218115},\n}\n\n\n\n

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\n \n\n \n \n Whitman, I. R; Vittinghoff, E.; deFilippi , C. R; Gottdiener, J. S; Alonso, A.; Psaty, B. M; Heckbert, S. R; Hoogeveen, R. C; Arking, D. E; Selvin, E.; Chen, L. Y; Dewland, T. A; and Marcus, G. M\n\n\n \n \n \n \n NT -pro BNP as a Mediator of the Racial Difference in Incident Atrial Fibrillation and Heart Failure.\n \n \n \n\n\n \n\n\n\n J Am Heart Assoc, 8: e010868. April 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{whitman_nt_2019,\n\ttitle = {{NT} -pro {BNP} as a {Mediator} of the {Racial} {Difference} in {Incident} {Atrial} {Fibrillation} and {Heart} {Failure}.},\n\tvolume = {8},\n\tissn = {2047-9980},\n\tdoi = {10.1161/JAHA.118.010868},\n\tabstract = {{\\textless}p{\\textgreater}Background Blacks harbor more cardiovascular risk factors than whites, but experience less atrial fibrillation ( AF ). Conversely, whites may have a lower risk of heart failure ( CHF ). N-terminal pro-B-type natriuretic peptide ( NT -pro BNP) levels are higher in whites, predict incident AF , and have diuretic effects in the setting of increased ventricular diastolic pressures, potentially providing a unifying explanation for these racial differences. Methods and Results We used data from the CHS (Cardiovascular Health Study) to determine the degree to which baseline NT -pro BNP levels mediate the relationships between race and incident AF and CHF by comparing beta estimates between models with and without NT -pro BNP . The ARIC (Atherosclerosis Risk in Communities) study was used to assess reproducibility. Among 4731 CHS (770 black) and 12 418 ARIC (3091 black) participants, there were 1277 and 1253 incident AF events, respectively. Whites had higher baseline NT -pro BNP ( CHS : 40\\% higher than blacks; 95\\% CI , 29-53; ARIC : 39\\% higher; 95\\% CI , 33-46) and had a greater risk of incident AF compared with blacks ( CHS : adjusted hazard ratio, 1.60; 95\\% CI , 1.31-1.93; ARIC : hazard ratio, 1.93; 95\\% CI , 1.57-2.27). NT -pro BNP levels explained a significant proportion of the racial difference in AF risk ( CHS : 36.2\\%; 95\\% CI , 23.2-69.2\\%; ARIC : 24.6\\%; 95\\% CI , 14.8-39.6\\%). Contrary to our hypothesis, given an increased risk of CHF among whites in CHS (adjusted hazard ratio, 1.20; 95\\% CI , 1.05-1.47) and the absence of a significant association between race and CHF in ARIC (adjusted hazard ratio, 1.07; 95\\% CI , 0.94-1.23), CHF -related mediation analyses were not performed. Conclusions A substantial portion of the relationship between race and AF was statistically explained by baseline NT -pro BNP levels. No consistent relationship between race and CHF was observed.{\\textless}/p{\\textgreater}},\n\tjournal = {J Am Heart Assoc},\n\tauthor = {Whitman, Isaac R and Vittinghoff, Eric and deFilippi, Christopher R and Gottdiener, John S and Alonso, Alvaro and Psaty, Bruce M and Heckbert, Susan R and Hoogeveen, Ron C and Arking, Dan E and Selvin, Elizabeth and Chen, Lin Y and Dewland, Thomas A and Marcus, Gregory M},\n\tmonth = apr,\n\tyear = {2019},\n\tpages = {e010868},\n}\n\n\n\n

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\n \n\n \n \n Jordan, D. M; Choi, H. K; Verbanck, M.; Topless, R.; Won, H.; Nadkarni, G.; Merriman, T. R; and Do, R.\n\n\n \n \n \n \n No causal effects of serum urate levels on the risk of chronic kidney disease: A Mendelian randomization study.\n \n \n \n\n\n \n\n\n\n PLoS Med, 16: e1002725. 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{jordan_no_2019,\n\ttitle = {No causal effects of serum urate levels on the risk of chronic kidney disease: {A} {Mendelian} randomization study.},\n\tvolume = {16},\n\tissn = {1549-1676},\n\tdoi = {10.1371/journal.pmed.1002725},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{BACKGROUND: }Studies have shown strong positive associations between serum urate (SU) levels and chronic kidney disease (CKD) risk; however, whether the relation is causal remains uncertain. We evaluate whether genetic data are consistent with a causal impact of SU level on the risk of CKD and estimated glomerular filtration rate (eGFR).{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS AND FINDINGS: }We used Mendelian randomization (MR) methods to evaluate the presence of a causal effect. We used aggregated genome-wide association data (N = 110,347 for SU, N = 69,374 for gout, N = 133,413 for eGFR, N = 117,165 for CKD), electronic-medical-record-linked UK Biobank data (N = 335,212), and population-based cohorts (N = 13,425), all in individuals of European ancestry, for SU levels and CKD. Our MR analysis showed that SU has a causal effect on neither eGFR level nor CKD risk across all MR analyses (all P {\\textgreater} 0.05). These null associations contrasted with our epidemiological association findings from the 4 population-based cohorts (change in eGFR level per 1-mg/dl [59.48 μmol/l] increase in SU: -1.99 ml/min/1.73 m2; 95\\% CI -2.86 to -1.11; P = 8.08 × 10(-6); odds ratio [OR] for CKD: 1.48; 95\\% CI 1.32 to 1.65; P = 1.52 × 10(-11)). In contrast, the same MR approaches showed that SU has a causal effect on the risk of gout (OR estimates ranging from 3.41 to 6.04 per 1-mg/dl increase in SU, all P {\\textless} 10-3), which served as a positive control of our approach. Overall, our MR analysis had {\\textgreater}99\\% power to detect a causal effect of SU level on the risk of CKD of the same magnitude as the observed epidemiological association between SU and CKD. Limitations of this study include the lifelong effect of a genetic perturbation not being the same as an acute perturbation, the inability to study non-European populations, and some sample overlap between the datasets used in the study.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSIONS: }Evidence from our series of causal inference approaches using genetics does not support a causal effect of SU level on eGFR level or CKD risk. Reducing SU levels is unlikely to reduce the risk of CKD development.{\\textless}/p{\\textgreater}},\n\tjournal = {PLoS Med},\n\tauthor = {Jordan, Daniel M and Choi, Hyon K and Verbanck, Marie and Topless, Ruth and Won, Hong-Hee and Nadkarni, Girish and Merriman, Tony R and Do, Ron},\n\tyear = {2019},\n\tkeywords = {Adult, Age Factors, Chronic, Female, Genome-Wide Association Study, Glomerular Filtration Rate, Humans, Male, Mendelian Randomization Analysis, Renal Insufficiency, Sex Factors, Uric Acid, Young Adult},\n\tpages = {e1002725},\n}\n\n\n\n

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\n \\textlessp\\textgreater\\textbfBACKGROUND: Studies have shown strong positive associations between serum urate (SU) levels and chronic kidney disease (CKD) risk; however, whether the relation is causal remains uncertain. We evaluate whether genetic data are consistent with a causal impact of SU level on the risk of CKD and estimated glomerular filtration rate (eGFR).\\textless/p\\textgreater\\textlessp\\textgreater\\textbfMETHODS AND FINDINGS: We used Mendelian randomization (MR) methods to evaluate the presence of a causal effect. We used aggregated genome-wide association data (N = 110,347 for SU, N = 69,374 for gout, N = 133,413 for eGFR, N = 117,165 for CKD), electronic-medical-record-linked UK Biobank data (N = 335,212), and population-based cohorts (N = 13,425), all in individuals of European ancestry, for SU levels and CKD. Our MR analysis showed that SU has a causal effect on neither eGFR level nor CKD risk across all MR analyses (all P \\textgreater 0.05). These null associations contrasted with our epidemiological association findings from the 4 population-based cohorts (change in eGFR level per 1-mg/dl [59.48 μmol/l] increase in SU: -1.99 ml/min/1.73 m2; 95% CI -2.86 to -1.11; P = 8.08 × 10(-6); odds ratio [OR] for CKD: 1.48; 95% CI 1.32 to 1.65; P = 1.52 × 10(-11)). In contrast, the same MR approaches showed that SU has a causal effect on the risk of gout (OR estimates ranging from 3.41 to 6.04 per 1-mg/dl increase in SU, all P \\textless 10-3), which served as a positive control of our approach. Overall, our MR analysis had \\textgreater99% power to detect a causal effect of SU level on the risk of CKD of the same magnitude as the observed epidemiological association between SU and CKD. Limitations of this study include the lifelong effect of a genetic perturbation not being the same as an acute perturbation, the inability to study non-European populations, and some sample overlap between the datasets used in the study.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfCONCLUSIONS: Evidence from our series of causal inference approaches using genetics does not support a causal effect of SU level on eGFR level or CKD risk. Reducing SU levels is unlikely to reduce the risk of CKD development.\\textless/p\\textgreater\n

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\n \n\n \n \n Pollack, S.; Igo, R. P; Jensen, R. A; Christiansen, M.; Li, X.; Cheng, C.; Ng, M. C Y; Smith, A. V; Rossin, E. J; Segrè, A. V; Davoudi, S.; Tan, G. S; Chen, Y. I.; Kuo, J. Z; Dimitrov, L. M; Stanwyck, L. K; Meng, W.; Hosseini, S M.; Imamura, M.; Nousome, D.; Kim, J.; Hai, Y.; Jia, Y.; Ahn, J.; Leong, A.; Shah, K.; Park, K. H.; Guo, X.; Ipp, E.; Taylor, K. D; Adler, S. G; Sedor, J. R; Freedman, B. I; Lee, I.; Sheu, W. H.; Kubo, M.; Takahashi, A.; Hadjadj, S.; Marre, M.; Trégouët, D.; McKean-Cowdin, R.; Varma, R.; McCarthy, M. I; Groop, L.; Ahlqvist, E.; Lyssenko, V.; Agardh, E.; Morris, A.; Doney, A. S F; Colhoun, H. M; Toppila, I.; Sandholm, N.; Groop, P.; Maeda, S.; Hanis, C. L; Penman, A.; Chen, C. J; Hancock, H.; Mitchell, P.; Craig, J. E; Chew, E. Y; Paterson, A. D; Grassi, M. A; Palmer, C.; Bowden, D. W; Yaspan, B. L; Siscovick, D.; Cotch, M. F.; Wang, J. J.; Burdon, K. P; Wong, T. Y; Klein, B. E K; Klein, R.; Rotter, J. I; Iyengar, S. K; Price, A. L; and Sobrin, L.\n\n\n \n \n \n \n Multiethnic Genome-Wide Association Study of Diabetic Retinopathy Using Liability Threshold Modeling of Duration of Diabetes and Glycemic Control.\n \n \n \n\n\n \n\n\n\n Diabetes, 68: 441–456. February 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{pollack_multiethnic_2019,\n\ttitle = {Multiethnic {Genome}-{Wide} {Association} {Study} of {Diabetic} {Retinopathy} {Using} {Liability} {Threshold} {Modeling} of {Duration} of {Diabetes} and {Glycemic} {Control}.},\n\tvolume = {68},\n\tissn = {1939-327X},\n\tdoi = {10.2337/db18-0567},\n\tabstract = {{\\textless}p{\\textgreater}To identify genetic variants associated with diabetic retinopathy (DR), we performed a large multiethnic genome-wide association study. Discovery included eight European cohorts ( = 3,246) and seven African American cohorts ( = 2,611). We meta-analyzed across cohorts using inverse-variance weighting, with and without liability threshold modeling of glycemic control and duration of diabetes. Variants with a value {\\textless}1 × 10 were investigated in replication cohorts that included 18,545 European, 16,453 Asian, and 2,710 Hispanic subjects. After correction for multiple testing, the C allele of rs142293996 in an intron of nuclear VCP-like () was associated with DR in European discovery cohorts ( = 2.1 × 10), but did not reach genome-wide significance after meta-analysis with replication cohorts. We applied the Disease Association Protein-Protein Link Evaluator (DAPPLE) to our discovery results to test for evidence of risk being spread across underlying molecular pathways. One protein-protein interaction network built from genes in regions associated with proliferative DR was found to have significant connectivity ( = 0.0009) and corroborated with gene set enrichment analyses. These findings suggest that genetic variation in as well as variation within a protein-protein interaction network that includes genes implicated in inflammation, may influence risk for DR.{\\textless}/p{\\textgreater}},\n\tjournal = {Diabetes},\n\tauthor = {Pollack, Samuela and Igo, Robert P and Jensen, Richard A and Christiansen, Mark and Li, Xiaohui and Cheng, Ching-Yu and Ng, Maggie C Y and Smith, Albert V and Rossin, Elizabeth J and Segrè, Ayellet V and Davoudi, Samaneh and Tan, Gavin S and Chen, Yii-Der Ida and Kuo, Jane Z and Dimitrov, Latchezar M and Stanwyck, Lynn K and Meng, Weihua and Hosseini, S Mohsen and Imamura, Minako and Nousome, Darryl and Kim, Jihye and Hai, Yang and Jia, Yucheng and Ahn, Jeeyun and Leong, Aaron and Shah, Kaanan and Park, Kyu Hyung and Guo, Xiuqing and Ipp, Eli and Taylor, Kent D and Adler, Sharon G and Sedor, John R and Freedman, Barry I and Lee, I-Te and Sheu, Wayne H-H and Kubo, Michiaki and Takahashi, Atsushi and Hadjadj, Samy and Marre, Michel and Trégouët, David-Alexandre and McKean-Cowdin, Roberta and Varma, Rohit and McCarthy, Mark I and Groop, Leif and Ahlqvist, Emma and Lyssenko, Valeriya and Agardh, Elisabet and Morris, Andrew and Doney, Alex S F and Colhoun, Helen M and Toppila, Iiro and Sandholm, Niina and Groop, Per-Henrik and Maeda, Shiro and Hanis, Craig L and Penman, Alan and Chen, Ching J and Hancock, Heather and Mitchell, Paul and Craig, Jamie E and Chew, Emily Y and Paterson, Andrew D and Grassi, Michael A and Palmer, Colin and Bowden, Donald W and Yaspan, Brian L and Siscovick, David and Cotch, Mary Frances and Wang, Jie Jin and Burdon, Kathryn P and Wong, Tien Y and Klein, Barbara E K and Klein, Ronald and Rotter, Jerome I and Iyengar, Sudha K and Price, Alkes L and Sobrin, Lucia},\n\tmonth = feb,\n\tyear = {2019},\n\tpages = {441--456},\n}\n\n\n\n

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\n \n\n \n \n Kilpeläinen, T. O; Bentley, A. R; Noordam, R.; Sung, Y. J.; Schwander, K.; Winkler, T. W; Jakupović, H.; Chasman, D. I; Manning, A.; Ntalla, I.; Aschard, H.; Brown, M. R; de Las Fuentes, L.; Franceschini, N.; Guo, X.; Vojinovic, D.; Aslibekyan, S.; Feitosa, M. F; Kho, M.; Musani, S. K; Richard, M.; Wang, H.; Wang, Z.; Bartz, T. M; Bielak, L. F; Campbell, A.; Dorajoo, R.; Fisher, V.; Hartwig, F. P; Horimoto, A. R V R; Li, C.; Lohman, K. K; Marten, J.; Sim, X.; Smith, A. V; Tajuddin, S. M; Alver, M.; Amini, M.; Boissel, M.; Chai, J. F.; Chen, X.; Divers, J.; Evangelou, E.; Gao, C.; Graff, M.; Harris, S. E; He, M.; Hsu, F.; Jackson, A. U; Zhao, J. H.; Kraja, A. T; Kuhnel, B.; Laguzzi, F.; Lyytikäinen, L.; Nolte, I. M; Rauramaa, R.; Riaz, M.; Robino, A.; Rueedi, R.; Stringham, H. M; Takeuchi, F.; van der Most, P. J; Varga, T. V; Verweij, N.; Ware, E. B; Wen, W.; Li, X.; Yanek, L. R; Amin, N.; Arnett, D. K; Boerwinkle, E.; Brumat, M.; Cade, B.; Canouil, M.; Chen, Y. I.; Concas, M. P.; Connell, J.; de Mutsert, R.; de Silva, H J.; de Vries, P. S; Demirkan, A.; Ding, J.; Eaton, C. B; Faul, J. D; Friedlander, Y.; Gabriel, K. P; Ghanbari, M.; Giulianini, F.; Gu, C. C.; Gu, D.; Harris, T. B; He, J.; Heikkinen, S.; Heng, C.; Hunt, S. C; Ikram, M A.; Jonas, J. B; Koh, W.; Komulainen, P.; Krieger, J. E; Kritchevsky, S. B; Kutalik, Z.; Kuusisto, J.; Langefeld, C. D; Langenberg, C.; Launer, L. J; Leander, K.; Lemaitre, R. N; Lewis, C. E; Liang, J.; Liu, J.; Mägi, R.; Manichaikul, A.; Meitinger, T.; Metspalu, A.; Milaneschi, Y.; Mohlke, K. L; Mosley, T. H; Murray, A. D; Nalls, M. A; Nang, E. K.; Nelson, C. P; Nona, S.; Norris, J. M; Nwuba, C. V.; O’Connell, J.; Palmer, N. D; Papanicolau, G. J; Pazoki, R.; Pedersen, N. L; Peters, A.; Peyser, P. A; Polasek, O.; Porteous, D. J; Poveda, A.; Raitakari, O. T; Rich, S. S; Risch, N.; Robinson, J. G; Rose, L. M; Rudan, I.; Schreiner, P. J; Scott, R. A; Sidney, S. S; Sims, M.; Smith, J. A; Snieder, H.; Sofer, T.; Starr, J. M; Sternfeld, B.; Strauch, K.; Tang, H.; Taylor, K. D; Tsai, M. Y; Tuomilehto, J.; Uitterlinden, A. G; van der Ende, M Y.; van Heemst, D.; Voortman, T.; Waldenberger, M.; Wennberg, P.; Wilson, G.; Xiang, Y.; Yao, J.; Yu, C.; Yuan, J.; Zhao, W.; Zonderman, A. B; Becker, D. M; Boehnke, M.; Bowden, D. W; de Faire, U.; Deary, I. J; Elliott, P.; Esko, T.; Freedman, B. I; Froguel, P.; Gasparini, P.; Gieger, C.; Kato, N.; Laakso, M.; Lakka, T. A; Lehtimäki, T.; Magnusson, P. K E; Oldehinkel, A. J; Penninx, B. W J H; Samani, N. J; Shu, X.; van der Harst, P.; van Vliet-Ostaptchouk, J. V; Vollenweider, P.; Wagenknecht, L. E; Wang, Y. X; Wareham, N. J; Weir, D. R; Wu, T.; Zheng, W.; Zhu, X.; Evans, M. K; Franks, P. W; Gudnason, V.; Hayward, C.; Horta, B. L; Kelly, T. N; Liu, Y.; North, K. E; Pereira, A. C; Ridker, P. M; Tai, E S.; van Dam, R. M; Fox, E. R; Kardia, S. L R; Liu, C.; Mook-Kanamori, D. O; Province, M. A; Redline, S.; van Duijn, C. M; Rotter, J. I; Kooperberg, C. B; Gauderman, W J.; Psaty, B. M; Rice, K.; Munroe, P. B; Fornage, M.; Cupples, L A.; Rotimi, C. N; Morrison, A. C; Rao, D. C; and Loos, R. J F\n\n\n \n \n \n \n Multi-ancestry study of blood lipid levels identifies four loci interacting with physical activity.\n \n \n \n\n\n \n\n\n\n Nat Commun, 10: 376. 2019.\n \n\n\n\n
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@article{kilpelainen_multi-ancestry_2019,\n\ttitle = {Multi-ancestry study of blood lipid levels identifies four loci interacting with physical activity.},\n\tvolume = {10},\n\tissn = {2041-1723},\n\tdoi = {10.1038/s41467-018-08008-w},\n\tabstract = {{\\textless}p{\\textgreater}Many genetic loci affect circulating lipid levels, but it remains unknown whether lifestyle factors, such as physical activity, modify these genetic effects. To identify lipid loci interacting with physical activity, we performed genome-wide analyses of circulating HDL cholesterol, LDL cholesterol, and triglyceride levels in up to 120,979 individuals of European, African, Asian, Hispanic, and Brazilian ancestry, with follow-up of suggestive associations in an additional 131,012 individuals. We find four loci, in/near CLASP1, LHX1, SNTA1, and CNTNAP2, that are associated with circulating lipid levels through interaction with physical activity; higher levels of physical activity enhance the HDL cholesterol-increasing effects of the CLASP1, LHX1, and SNTA1 loci and attenuate the LDL cholesterol-increasing effect of the CNTNAP2 locus. The CLASP1, LHX1, and SNTA1 regions harbor genes linked to muscle function and lipid metabolism. Our results elucidate the role of physical activity interactions in the genetic contribution to blood lipid levels.{\\textless}/p{\\textgreater}},\n\tjournal = {Nat Commun},\n\tauthor = {Kilpeläinen, Tuomas O and Bentley, Amy R and Noordam, Raymond and Sung, Yun Ju and Schwander, Karen and Winkler, Thomas W and Jakupović, Hermina and Chasman, Daniel I and Manning, Alisa and Ntalla, Ioanna and Aschard, Hugues and Brown, Michael R and de Las Fuentes, Lisa and Franceschini, Nora and Guo, Xiuqing and Vojinovic, Dina and Aslibekyan, Stella and Feitosa, Mary F and Kho, Minjung and Musani, Solomon K and Richard, Melissa and Wang, Heming and Wang, Zhe and Bartz, Traci M and Bielak, Lawrence F and Campbell, Archie and Dorajoo, Rajkumar and Fisher, Virginia and Hartwig, Fernando P and Horimoto, Andrea R V R and Li, Changwei and Lohman, Kurt K and Marten, Jonathan and Sim, Xueling and Smith, Albert V and Tajuddin, Salman M and Alver, Maris and Amini, Marzyeh and Boissel, Mathilde and Chai, Jin Fang and Chen, Xu and Divers, Jasmin and Evangelou, Evangelos and Gao, Chuan and Graff, Mariaelisa and Harris, Sarah E and He, Meian and Hsu, Fang-Chi and Jackson, Anne U and Zhao, Jing Hua and Kraja, Aldi T and Kuhnel, Brigitte and Laguzzi, Federica and Lyytikäinen, Leo-Pekka and Nolte, Ilja M and Rauramaa, Rainer and Riaz, Muhammad and Robino, Antonietta and Rueedi, Rico and Stringham, Heather M and Takeuchi, Fumihiko and van der Most, Peter J and Varga, Tibor V and Verweij, Niek and Ware, Erin B and Wen, Wanqing and Li, Xiaoyin and Yanek, Lisa R and Amin, Najaf and Arnett, Donna K and Boerwinkle, Eric and Brumat, Marco and Cade, Brian and Canouil, Mickaël and Chen, Yii-Der Ida and Concas, Maria Pina and Connell, John and de Mutsert, Renée and de Silva, H Janaka and de Vries, Paul S and Demirkan, Ayse and Ding, Jingzhong and Eaton, Charles B and Faul, Jessica D and Friedlander, Yechiel and Gabriel, Kelley P and Ghanbari, Mohsen and Giulianini, Franco and Gu, Chi Charles and Gu, Dongfeng and Harris, Tamara B and He, Jiang and Heikkinen, Sami and Heng, Chew-Kiat and Hunt, Steven C and Ikram, M Arfan and Jonas, Jost B and Koh, Woon-Puay and Komulainen, Pirjo and Krieger, Jose E and Kritchevsky, Stephen B and Kutalik, Zoltán and Kuusisto, Johanna and Langefeld, Carl D and Langenberg, Claudia and Launer, Lenore J and Leander, Karin and Lemaitre, Rozenn N and Lewis, Cora E and Liang, Jingjing and Liu, Jianjun and Mägi, Reedik and Manichaikul, Ani and Meitinger, Thomas and Metspalu, Andres and Milaneschi, Yuri and Mohlke, Karen L and Mosley, Thomas H and Murray, Alison D and Nalls, Mike A and Nang, Ei-Ei Khaing and Nelson, Christopher P and Nona, Sotoodehnia and Norris, Jill M and Nwuba, Chiamaka Vivian and O’Connell, Jeff and Palmer, Nicholette D and Papanicolau, George J and Pazoki, Raha and Pedersen, Nancy L and Peters, Annette and Peyser, Patricia A and Polasek, Ozren and Porteous, David J and Poveda, Alaitz and Raitakari, Olli T and Rich, Stephen S and Risch, Neil and Robinson, Jennifer G and Rose, Lynda M and Rudan, Igor and Schreiner, Pamela J and Scott, Robert A and Sidney, Stephen S and Sims, Mario and Smith, Jennifer A and Snieder, Harold and Sofer, Tamar and Starr, John M and Sternfeld, Barbara and Strauch, Konstantin and Tang, Hua and Taylor, Kent D and Tsai, Michael Y and Tuomilehto, Jaakko and Uitterlinden, André G and van der Ende, M Yldau and van Heemst, Diana and Voortman, Trudy and Waldenberger, Melanie and Wennberg, Patrik and Wilson, Gregory and Xiang, Yong-Bing and Yao, Jie and Yu, Caizheng and Yuan, Jian-Min and Zhao, Wei and Zonderman, Alan B and Becker, Diane M and Boehnke, Michael and Bowden, Donald W and de Faire, Ulf and Deary, Ian J and Elliott, Paul and Esko, Tõnu and Freedman, Barry I and Froguel, Philippe and Gasparini, Paolo and Gieger, Christian and Kato, Norihiro and Laakso, Markku and Lakka, Timo A and Lehtimäki, Terho and Magnusson, Patrik K E and Oldehinkel, Albertine J and Penninx, Brenda W J H and Samani, Nilesh J and Shu, Xiao-Ou and van der Harst, Pim and van Vliet-Ostaptchouk, Jana V and Vollenweider, Peter and Wagenknecht, Lynne E and Wang, Ya X and Wareham, Nicholas J and Weir, David R and Wu, Tangchun and Zheng, Wei and Zhu, Xiaofeng and Evans, Michele K and Franks, Paul W and Gudnason, Vilmundur and Hayward, Caroline and Horta, Bernardo L and Kelly, Tanika N and Liu, Yongmei and North, Kari E and Pereira, Alexandre C and Ridker, Paul M and Tai, E Shyong and van Dam, Rob M and Fox, Ervin R and Kardia, Sharon L R and Liu, Ching-Ti and Mook-Kanamori, Dennis O and Province, Michael A and Redline, Susan and van Duijn, Cornelia M and Rotter, Jerome I and Kooperberg, Charles B and Gauderman, W James and Psaty, Bruce M and Rice, Kenneth and Munroe, Patricia B and Fornage, Myriam and Cupples, L Adrienne and Rotimi, Charles N and Morrison, Alanna C and Rao, Dabeeru C and Loos, Ruth J F},\n\tyear = {2019},\n\tkeywords = {80 and over, Adolescent, Adult, African Continental Ancestry Group, Aged, Asian Continental Ancestry Group, Brazil, Calcium-Binding Proteins, Cholesterol, European Continental Ancestry Group, Exercise, Female, Genetic Loci, Genome-Wide Association Study, Genotype, HDL, Hispanic Americans, Humans, LDL, LIM-Homeodomain Proteins, Lipid Metabolism, Lipids, Male, Membrane Proteins, Microtubule-Associated Proteins, Middle Aged, Muscle Proteins, Nerve Tissue Proteins, Transcription Factors, Triglycerides, Young Adult},\n\tpages = {376},\n}\n\n\n\n

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\n \n\n \n \n Noordam, R.; Bos, M. M; Wang, H.; Winkler, T. W; Bentley, A. R; Kilpeläinen, T. O; de Vries, P. S; Sung, Y. J.; Schwander, K.; Cade, B. E; Manning, A.; Aschard, H.; Brown, M. R; Chen, H.; Franceschini, N.; Musani, S. K; Richard, M.; Vojinovic, D.; Aslibekyan, S.; Bartz, T. M; de Las Fuentes, L.; Feitosa, M.; Horimoto, A. R; Ilkov, M.; Kho, M.; Kraja, A.; Li, C.; Lim, E.; Liu, Y.; Mook-Kanamori, D. O; Rankinen, T.; Tajuddin, S. M; van der Spek, A.; Wang, Z.; Marten, J.; Laville, V.; Alver, M.; Evangelou, E.; Graff, M. E; He, M.; Kuhnel, B.; Lyytikäinen, L.; Marques-Vidal, P.; Nolte, I. M; Palmer, N. D; Rauramaa, R.; Shu, X.; Snieder, H.; Weiss, S.; Wen, W.; Yanek, L. R; Adolfo, C.; Ballantyne, C.; Bielak, L.; Biermasz, N. R; Boerwinkle, E.; Dimou, N.; Eiriksdottir, G.; Gao, C.; Gharib, S. A; Gottlieb, D. J; Haba-Rubio, J.; Harris, T. B; Heikkinen, S.; Heinzer, R.; Hixson, J. E; Homuth, G.; Ikram, M A.; Komulainen, P.; Krieger, J. E; Lee, J.; Liu, J.; Lohman, K. K; Luik, A. I; Mägi, R.; Martin, L. W; Meitinger, T.; Metspalu, A.; Milaneschi, Y.; Nalls, M. A; O’Connell, J.; Peters, A.; Peyser, P.; Raitakari, O. T; Reiner, A. P; Rensen, P. C N; Rice, T. K; Rich, S. S; Roenneberg, T.; Rotter, J. I; Schreiner, P. J; Shikany, J.; Sidney, S. S; Sims, M.; Sitlani, C. M; Sofer, T.; Strauch, K.; Swertz, M. A; Taylor, K. D; Uitterlinden, A. G; van Duijn, C. M; Völzke, H.; Waldenberger, M.; Wallance, R. B; van Dijk, K. W.; Yu, C.; Zonderman, A. B; Becker, D. M; Elliott, P.; Esko, T.; Gieger, C.; Grabe, H. J; Lakka, T. A; Lehtimäki, T.; North, K. E; Penninx, B. W J H; Vollenweider, P.; Wagenknecht, L. E; Wu, T.; Xiang, Y.; Zheng, W.; Arnett, D. K; Bouchard, C.; Evans, M. K; Gudnason, V.; Kardia, S.; Kelly, T. N; Kritchevsky, S. B; Loos, R. J F; Pereira, A. C; Province, M.; Psaty, B. M; Rotimi, C.; Zhu, X.; Amin, N.; Cupples, L A.; Fornage, M.; Fox, E. F; Guo, X.; Gauderman, W J.; Rice, K.; Kooperberg, C.; Munroe, P. B; Liu, C.; Morrison, A. C; Rao, D. C; van Heemst, D.; and Redline, S.\n\n\n \n \n \n \n Multi-ancestry sleep-by-SNP interaction analysis in 126,926 individuals reveals lipid loci stratified by sleep duration.\n \n \n \n\n\n \n\n\n\n Nat Commun, 10: 5121. November 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{noordam_multi-ancestry_2019,\n\ttitle = {Multi-ancestry sleep-by-{SNP} interaction analysis in 126,926 individuals reveals lipid loci stratified by sleep duration.},\n\tvolume = {10},\n\tissn = {2041-1723},\n\tdoi = {10.1038/s41467-019-12958-0},\n\tabstract = {{\\textless}p{\\textgreater}Both short and long sleep are associated with an adverse lipid profile, likely through different biological pathways. To elucidate the biology of sleep-associated adverse lipid profile, we conduct multi-ancestry genome-wide sleep-SNP interaction analyses on three lipid traits (HDL-c, LDL-c and triglycerides). In the total study sample (discovery + replication) of 126,926 individuals from 5 different ancestry groups, when considering either long or short total sleep time interactions in joint analyses, we identify 49 previously unreported lipid loci, and 10 additional previously unreported lipid loci in a restricted sample of European-ancestry cohorts. In addition, we identify new gene-sleep interactions for known lipid loci such as LPL and PCSK9. The previously unreported lipid loci have a modest explained variance in lipid levels: most notable, gene-short-sleep interactions explain 4.25\\% of the variance in triglyceride level. Collectively, these findings contribute to our understanding of the biological mechanisms involved in sleep-associated adverse lipid profiles.{\\textless}/p{\\textgreater}},\n\tjournal = {Nat Commun},\n\tauthor = {Noordam, Raymond and Bos, Maxime M and Wang, Heming and Winkler, Thomas W and Bentley, Amy R and Kilpeläinen, Tuomas O and de Vries, Paul S and Sung, Yun Ju and Schwander, Karen and Cade, Brian E and Manning, Alisa and Aschard, Hugues and Brown, Michael R and Chen, Han and Franceschini, Nora and Musani, Solomon K and Richard, Melissa and Vojinovic, Dina and Aslibekyan, Stella and Bartz, Traci M and de Las Fuentes, Lisa and Feitosa, Mary and Horimoto, Andrea R and Ilkov, Marjan and Kho, Minjung and Kraja, Aldi and Li, Changwei and Lim, Elise and Liu, Yongmei and Mook-Kanamori, Dennis O and Rankinen, Tuomo and Tajuddin, Salman M and van der Spek, Ashley and Wang, Zhe and Marten, Jonathan and Laville, Vincent and Alver, Maris and Evangelou, Evangelos and Graff, Maria E and He, Meian and Kuhnel, Brigitte and Lyytikäinen, Leo-Pekka and Marques-Vidal, Pedro and Nolte, Ilja M and Palmer, Nicholette D and Rauramaa, Rainer and Shu, Xiao-Ou and Snieder, Harold and Weiss, Stefan and Wen, Wanqing and Yanek, Lisa R and Adolfo, Correa and Ballantyne, Christie and Bielak, Larry and Biermasz, Nienke R and Boerwinkle, Eric and Dimou, Niki and Eiriksdottir, Gudny and Gao, Chuan and Gharib, Sina A and Gottlieb, Daniel J and Haba-Rubio, José and Harris, Tamara B and Heikkinen, Sami and Heinzer, Raphael and Hixson, James E and Homuth, Georg and Ikram, M Arfan and Komulainen, Pirjo and Krieger, Jose E and Lee, Jiwon and Liu, Jingmin and Lohman, Kurt K and Luik, Annemarie I and Mägi, Reedik and Martin, Lisa W and Meitinger, Thomas and Metspalu, Andres and Milaneschi, Yuri and Nalls, Mike A and O’Connell, Jeff and Peters, Annette and Peyser, Patricia and Raitakari, Olli T and Reiner, Alex P and Rensen, Patrick C N and Rice, Treva K and Rich, Stephen S and Roenneberg, Till and Rotter, Jerome I and Schreiner, Pamela J and Shikany, James and Sidney, Stephen S and Sims, Mario and Sitlani, Colleen M and Sofer, Tamar and Strauch, Konstantin and Swertz, Morris A and Taylor, Kent D and Uitterlinden, André G and van Duijn, Cornelia M and Völzke, Henry and Waldenberger, Melanie and Wallance, Robert B and van Dijk, Ko Willems and Yu, Caizheng and Zonderman, Alan B and Becker, Diane M and Elliott, Paul and Esko, Tõnu and Gieger, Christian and Grabe, Hans J and Lakka, Timo A and Lehtimäki, Terho and North, Kari E and Penninx, Brenda W J H and Vollenweider, Peter and Wagenknecht, Lynne E and Wu, Tangchun and Xiang, Yong-Bing and Zheng, Wei and Arnett, Donna K and Bouchard, Claude and Evans, Michele K and Gudnason, Vilmundur and Kardia, Sharon and Kelly, Tanika N and Kritchevsky, Stephen B and Loos, Ruth J F and Pereira, Alexandre C and Province, Mike and Psaty, Bruce M and Rotimi, Charles and Zhu, Xiaofeng and Amin, Najaf and Cupples, L Adrienne and Fornage, Myriam and Fox, Ervin F and Guo, Xiuqing and Gauderman, W James and Rice, Kenneth and Kooperberg, Charles and Munroe, Patricia B and Liu, Ching-Ti and Morrison, Alanna C and Rao, Dabeeru C and van Heemst, Diana and Redline, Susan},\n\tmonth = nov,\n\tyear = {2019},\n\tpages = {5121},\n}\n\n\n\n

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\n \n\n \n \n Bentley, A. R; Sung, Y. J; Brown, M. R; Winkler, T. W; Kraja, A. T; Ntalla, I.; Schwander, K.; Chasman, D. I; Lim, E.; Deng, X.; Guo, X.; Liu, J.; Lu, Y.; Cheng, C.; Sim, X.; Vojinovic, D.; Huffman, J. E; Musani, S. K; Li, C.; Feitosa, M. F; Richard, M. A; Noordam, R.; Baker, J.; Chen, G.; Aschard, H.; Bartz, T. M; Ding, J.; Dorajoo, R.; Manning, A. K; Rankinen, T.; Smith, A. V; Tajuddin, S. M; Zhao, W.; Graff, M.; Alver, M.; Boissel, M.; Chai, J. F.; Chen, X.; Divers, J.; Evangelou, E.; Gao, C.; Goel, A.; Hagemeijer, Y.; Harris, S. E; Hartwig, F. P; He, M.; Horimoto, A. R V R; Hsu, F.; Hung, Y.; Jackson, A. U; Kasturiratne, A.; Komulainen, P.; Kuhnel, B.; Leander, K.; Lin, K.; Luan, J.; Lyytikäinen, L.; Matoba, N.; Nolte, I. M; Pietzner, M.; Prins, B.; Riaz, M.; Robino, A.; Said, M A.; Schupf, N.; Scott, R. A; Sofer, T.; Stančáková, A.; Takeuchi, F.; Tayo, B. O; van der Most, P. J; Varga, T. V; Wang, T.; Wang, Y.; Ware, E. B; Wen, W.; Xiang, Y.; Yanek, L. R; Zhang, W.; Zhao, J. H.; Adeyemo, A.; Afaq, S.; Amin, N.; Amini, M.; Arking, D. E; Arzumanyan, Z.; Aung, T.; Ballantyne, C.; Barr, R G.; Bielak, L. F; Boerwinkle, E.; Bottinger, E. P; Broeckel, U.; Brown, M.; Cade, B. E; Campbell, A.; Canouil, M.; Charumathi, S.; Chen, Y. I.; Christensen, K.; Concas, M. P.; Connell, J. M; de Las Fuentes, L.; de Silva, H J.; de Vries, P. S; Doumatey, A.; Duan, Q.; Eaton, C. B; Eppinga, R. N; Faul, J. D; Floyd, J. S; Forouhi, N. G; Forrester, T.; Friedlander, Y.; Gandin, I.; Gao, H.; Ghanbari, M.; Gharib, S. A; Gigante, B.; Giulianini, F.; Grabe, H. J; Gu, C C.; Harris, T. B; Heikkinen, S.; Heng, C.; Hirata, M.; Hixson, J. E; Ikram, M A.; Jia, Y.; Joehanes, R.; Johnson, C.; Jonas, J. B.; Justice, A. E; Katsuya, T.; Khor, C. C.; Kilpeläinen, T. O; Koh, W.; Kolcic, I.; Kooperberg, C.; Krieger, J. E; Kritchevsky, S. B; Kubo, M.; Kuusisto, J.; Lakka, T. A; Langefeld, C. D; Langenberg, C.; Launer, L. J; Lehne, B.; Lewis, C. E; Li, Y.; Liang, J.; Lin, S.; Liu, C.; Liu, J.; Liu, K.; Loh, M.; Lohman, K. K; Louie, T.; Luzzi, A.; Mägi, R.; Mahajan, A.; Manichaikul, A. W; McKenzie, C. A; Meitinger, T.; Metspalu, A.; Milaneschi, Y.; Milani, L.; Mohlke, K. L; Momozawa, Y.; Morris, A. P; Murray, A. D; Nalls, M. A; Nauck, M.; Nelson, C. P; North, K. E; O’Connell, J. R; Palmer, N. D; Papanicolau, G. J; Pedersen, N. L; Peters, A.; Peyser, P. A; Polasek, O.; Poulter, N.; Raitakari, O. T; Reiner, A. P; Renstrom, F.; Rice, T. K; Rich, S. S; Robinson, J. G; Rose, L. M; Rosendaal, F. R; Rudan, I.; Schmidt, C. O; Schreiner, P. J; Scott, W. R; Sever, P.; Shi, Y.; Sidney, S.; Sims, M.; Smith, J. A; Snieder, H.; Starr, J. M; Strauch, K.; Stringham, H. M; Tan, N. Y Q; Tang, H.; Taylor, K. D; Teo, Y. Y.; Tham, Y. C.; Tiemeier, H.; Turner, S. T; Uitterlinden, A. G; van Heemst, D.; Waldenberger, M.; Wang, H.; Wang, L.; Wang, L.; Wei, W. B.; Williams, C. A; Wilson, G.; Wojczynski, M. K; Yao, J.; Young, K.; Yu, C.; Yuan, J.; Zhou, J.; Zonderman, A. B; Becker, D. M; Boehnke, M.; Bowden, D. W; Chambers, J. C; Cooper, R. S; de Faire, U.; Deary, I. J; Elliott, P.; Esko, T.; Farrall, M.; Franks, P. W; Freedman, B. I; Froguel, P.; Gasparini, P.; Gieger, C.; Horta, B. L; Juang, J. J.; Kamatani, Y.; Kammerer, C. M; Kato, N.; Kooner, J. S; Laakso, M.; Laurie, C. C; Lee, I.; Lehtimäki, T.; Magnusson, P. K E; Oldehinkel, A. J; Penninx, B. W J H; Pereira, A. C; Rauramaa, R.; Redline, S.; Samani, N. J; Scott, J.; Shu, X.; van der Harst, P.; Wagenknecht, L. E; Wang, J.; Wang, Y. X.; Wareham, N. J; Watkins, H.; Weir, D. R; Wickremasinghe, A. R; Wu, T.; Zeggini, E.; Zheng, W.; Bouchard, C.; Evans, M. K; Gudnason, V.; Kardia, S. L R; Liu, Y.; Psaty, B. M; Ridker, P. M; van Dam, R. M; Mook-Kanamori, D. O; Fornage, M.; Province, M. A; Kelly, T. N; Fox, E. R; Hayward, C.; van Duijn, C. M; Tai, E S.; Wong, T. Y.; Loos, R. J F; Franceschini, N.; Rotter, J. I; Zhu, X.; Bierut, L. J; Gauderman, W J.; Rice, K.; Munroe, P. B; Morrison, A. C; Rao, D. C; Rotimi, C. N; and Cupples, L A.\n\n\n \n \n \n \n Multi-ancestry genome-wide gene-smoking interaction study of 387,272 individuals identifies new loci associated with serum lipids.\n \n \n \n\n\n \n\n\n\n Nat Genet, 51: 636–648. April 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{bentley_multi-ancestry_2019,\n\ttitle = {Multi-ancestry genome-wide gene-smoking interaction study of 387,272 individuals identifies new loci associated with serum lipids.},\n\tvolume = {51},\n\tissn = {1546-1718},\n\tdoi = {10.1038/s41588-019-0378-y},\n\tabstract = {{\\textless}p{\\textgreater}The concentrations of high- and low-density-lipoprotein cholesterol and triglycerides are influenced by smoking, but it is unknown whether genetic associations with lipids may be modified by smoking. We conducted a multi-ancestry genome-wide gene-smoking interaction study in 133,805 individuals with follow-up in an additional 253,467 individuals. Combined meta-analyses identified 13 new loci associated with lipids, some of which were detected only because association differed by smoking status. Additionally, we demonstrate the importance of including diverse populations, particularly in studies of interactions with lifestyle factors, where genomic and lifestyle differences by ancestry may contribute to novel findings.{\\textless}/p{\\textgreater}},\n\tjournal = {Nat Genet},\n\tauthor = {Bentley, Amy R and Sung, Yun J and Brown, Michael R and Winkler, Thomas W and Kraja, Aldi T and Ntalla, Ioanna and Schwander, Karen and Chasman, Daniel I and Lim, Elise and Deng, Xuan and Guo, Xiuqing and Liu, Jingmin and Lu, Yingchang and Cheng, Ching-Yu and Sim, Xueling and Vojinovic, Dina and Huffman, Jennifer E and Musani, Solomon K and Li, Changwei and Feitosa, Mary F and Richard, Melissa A and Noordam, Raymond and Baker, Jenna and Chen, Guanjie and Aschard, Hugues and Bartz, Traci M and Ding, Jingzhong and Dorajoo, Rajkumar and Manning, Alisa K and Rankinen, Tuomo and Smith, Albert V and Tajuddin, Salman M and Zhao, Wei and Graff, Mariaelisa and Alver, Maris and Boissel, Mathilde and Chai, Jin Fang and Chen, Xu and Divers, Jasmin and Evangelou, Evangelos and Gao, Chuan and Goel, Anuj and Hagemeijer, Yanick and Harris, Sarah E and Hartwig, Fernando P and He, Meian and Horimoto, Andrea R V R and Hsu, Fang-Chi and Hung, Yi-Jen and Jackson, Anne U and Kasturiratne, Anuradhani and Komulainen, Pirjo and Kuhnel, Brigitte and Leander, Karin and Lin, Keng-Hung and Luan, Jian’an and Lyytikäinen, Leo-Pekka and Matoba, Nana and Nolte, Ilja M and Pietzner, Maik and Prins, Bram and Riaz, Muhammad and Robino, Antonietta and Said, M Abdullah and Schupf, Nicole and Scott, Robert A and Sofer, Tamar and Stančáková, Alena and Takeuchi, Fumihiko and Tayo, Bamidele O and van der Most, Peter J and Varga, Tibor V and Wang, Tzung-Dau and Wang, Yajuan and Ware, Erin B and Wen, Wanqing and Xiang, Yong-Bing and Yanek, Lisa R and Zhang, Weihua and Zhao, Jing Hua and Adeyemo, Adebowale and Afaq, Saima and Amin, Najaf and Amini, Marzyeh and Arking, Dan E and Arzumanyan, Zorayr and Aung, Tin and Ballantyne, Christie and Barr, R Graham and Bielak, Lawrence F and Boerwinkle, Eric and Bottinger, Erwin P and Broeckel, Ulrich and Brown, Morris and Cade, Brian E and Campbell, Archie and Canouil, Mickaël and Charumathi, Sabanayagam and Chen, Yii-Der Ida and Christensen, Kaare and Concas, Maria Pina and Connell, John M and de Las Fuentes, Lisa and de Silva, H Janaka and de Vries, Paul S and Doumatey, Ayo and Duan, Qing and Eaton, Charles B and Eppinga, Ruben N and Faul, Jessica D and Floyd, James S and Forouhi, Nita G and Forrester, Terrence and Friedlander, Yechiel and Gandin, Ilaria and Gao, He and Ghanbari, Mohsen and Gharib, Sina A and Gigante, Bruna and Giulianini, Franco and Grabe, Hans J and Gu, C Charles and Harris, Tamara B and Heikkinen, Sami and Heng, Chew-Kiat and Hirata, Makoto and Hixson, James E and Ikram, M Arfan and Jia, Yucheng and Joehanes, Roby and Johnson, Craig and Jonas, Jost Bruno and Justice, Anne E and Katsuya, Tomohiro and Khor, Chiea Chuen and Kilpeläinen, Tuomas O and Koh, Woon-Puay and Kolcic, Ivana and Kooperberg, Charles and Krieger, Jose E and Kritchevsky, Stephen B and Kubo, Michiaki and Kuusisto, Johanna and Lakka, Timo A and Langefeld, Carl D and Langenberg, Claudia and Launer, Lenore J and Lehne, Benjamin and Lewis, Cora E and Li, Yize and Liang, Jingjing and Lin, Shiow and Liu, Ching-Ti and Liu, Jianjun and Liu, Kiang and Loh, Marie and Lohman, Kurt K and Louie, Tin and Luzzi, Anna and Mägi, Reedik and Mahajan, Anubha and Manichaikul, Ani W and McKenzie, Colin A and Meitinger, Thomas and Metspalu, Andres and Milaneschi, Yuri and Milani, Lili and Mohlke, Karen L and Momozawa, Yukihide and Morris, Andrew P and Murray, Alison D and Nalls, Mike A and Nauck, Matthias and Nelson, Christopher P and North, Kari E and O’Connell, Jeffrey R and Palmer, Nicholette D and Papanicolau, George J and Pedersen, Nancy L and Peters, Annette and Peyser, Patricia A and Polasek, Ozren and Poulter, Neil and Raitakari, Olli T and Reiner, Alex P and Renstrom, Frida and Rice, Treva K and Rich, Stephen S and Robinson, Jennifer G and Rose, Lynda M and Rosendaal, Frits R and Rudan, Igor and Schmidt, Carsten O and Schreiner, Pamela J and Scott, William R and Sever, Peter and Shi, Yuan and Sidney, Stephen and Sims, Mario and Smith, Jennifer A and Snieder, Harold and Starr, John M and Strauch, Konstantin and Stringham, Heather M and Tan, Nicholas Y Q and Tang, Hua and Taylor, Kent D and Teo, Yik Ying and Tham, Yih Chung and Tiemeier, Henning and Turner, Stephen T and Uitterlinden, André G and van Heemst, Diana and Waldenberger, Melanie and Wang, Heming and Wang, Lan and Wang, Lihua and Wei, Wen Bin and Williams, Christine A and Wilson, Gregory and Wojczynski, Mary K and Yao, Jie and Young, Kristin and Yu, Caizheng and Yuan, Jian-Min and Zhou, Jie and Zonderman, Alan B and Becker, Diane M and Boehnke, Michael and Bowden, Donald W and Chambers, John C and Cooper, Richard S and de Faire, Ulf and Deary, Ian J and Elliott, Paul and Esko, Tõnu and Farrall, Martin and Franks, Paul W and Freedman, Barry I and Froguel, Philippe and Gasparini, Paolo and Gieger, Christian and Horta, Bernardo L and Juang, Jyh-Ming Jimmy and Kamatani, Yoichiro and Kammerer, Candace M and Kato, Norihiro and Kooner, Jaspal S and Laakso, Markku and Laurie, Cathy C and Lee, I-Te and Lehtimäki, Terho and Magnusson, Patrik K E and Oldehinkel, Albertine J and Penninx, Brenda W J H and Pereira, Alexandre C and Rauramaa, Rainer and Redline, Susan and Samani, Nilesh J and Scott, James and Shu, Xiao-Ou and van der Harst, Pim and Wagenknecht, Lynne E and Wang, Jun-Sing and Wang, Ya Xing and Wareham, Nicholas J and Watkins, Hugh and Weir, David R and Wickremasinghe, Ananda R and Wu, Tangchun and Zeggini, Eleftheria and Zheng, Wei and Bouchard, Claude and Evans, Michele K and Gudnason, Vilmundur and Kardia, Sharon L R and Liu, Yongmei and Psaty, Bruce M and Ridker, Paul M and van Dam, Rob M and Mook-Kanamori, Dennis O and Fornage, Myriam and Province, Michael A and Kelly, Tanika N and Fox, Ervin R and Hayward, Caroline and van Duijn, Cornelia M and Tai, E Shyong and Wong, Tien Yin and Loos, Ruth J F and Franceschini, Nora and Rotter, Jerome I and Zhu, Xiaofeng and Bierut, Laura J and Gauderman, W James and Rice, Kenneth and Munroe, Patricia B and Morrison, Alanna C and Rao, Dabeeru C and Rotimi, Charles N and Cupples, L Adrienne},\n\tmonth = apr,\n\tyear = {2019},\n\tpages = {636--648},\n}\n\n\n\n

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\n \n\n \n \n Lindström, S.; Brody, J. A; Turman, C.; Germain, M.; Bartz, T. M; Smith, E. N; Chen, M.; Puurunen, M.; Chasman, D.; Hassler, J.; Pankratz, N.; Basu, S.; Guan, W.; Gyorgy, B.; Ibrahim, M.; Empana, J.; Olaso, R.; Jackson, R.; Braekkan, S. K; McKnight, B.; Deleuze, J.; O’Donnell, C. J; Jouven, X.; Frazer, K. A; Psaty, B. M; Wiggins, K. L; Taylor, K.; Reiner, A. P; Heckbert, S. R; Kooperberg, C.; Ridker, P.; Hansen, J.; Tang, W.; Johnson, A. D; Morange, P.; Trégouët, D. A; Kraft, P.; Smith, N. L; and Kabrhel, C.\n\n\n \n \n \n \n A large-scale exome array analysis of venous thromboembolism.\n \n \n \n\n\n \n\n\n\n Genet Epidemiol. January 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{lindstrom_large-scale_2019,\n\ttitle = {A large-scale exome array analysis of venous thromboembolism.},\n\tissn = {1098-2272},\n\tdoi = {10.1002/gepi.22187},\n\tabstract = {{\\textless}p{\\textgreater}Although recent Genome-Wide Association Studies have identified novel associations for common variants, there has been no comprehensive exome-wide search for low-frequency variants that affect the risk of venous thromboembolism (VTE). We conducted a meta-analysis of 11 studies comprising 8,332 cases and 16,087 controls of European ancestry and 382 cases and 1,476 controls of African American ancestry genotyped with the Illumina HumanExome BeadChip. We used the seqMeta package in R to conduct single variant and gene-based rare variant tests. In the single variant analysis, we limited our analysis to the 64,794 variants with at least 40 minor alleles across studies (minor allele frequency [MAF] 0.08\\%). We confirmed associations with previously identified VTE loci, including ABO, F5, F11, and FGA. After adjusting for multiple testing, we observed no novel significant findings in single variant or gene-based analysis. Given our sample size, we had greater than 80\\% power to detect minimum odds ratios greater than 1.5 and 1.8 for a single variant with MAF of 0.01 and 0.005, respectively. Larger studies and sequence data may be needed to identify novel low-frequency and rare variants associated with VTE risk.{\\textless}/p{\\textgreater}},\n\tjournal = {Genet Epidemiol},\n\tauthor = {Lindström, Sara and Brody, Jennifer A and Turman, Constance and Germain, Marine and Bartz, Traci M and Smith, Erin N and Chen, Ming-Huei and Puurunen, Marja and Chasman, Daniel and Hassler, Jeffrey and Pankratz, Nathan and Basu, Saonli and Guan, Weihua and Gyorgy, Beata and Ibrahim, Manal and Empana, Jean-Philippe and Olaso, Robert and Jackson, Rebecca and Braekkan, Sigrid K and McKnight, Barbara and Deleuze, Jean-Francois and O’Donnell, Cristopher J and Jouven, Xavier and Frazer, Kelly A and Psaty, Bruce M and Wiggins, Kerri L and Taylor, Kent and Reiner, Alexander P and Heckbert, Susan R and Kooperberg, Charles and Ridker, Paul and Hansen, John-Bjarne and Tang, Weihong and Johnson, Andrew D and Morange, Pierre-Emmanuel and Trégouët, David A and Kraft, Peter and Smith, Nicholas L and Kabrhel, Christopher},\n\tmonth = jan,\n\tyear = {2019},\n}\n\n\n\n

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\n \n\n \n \n de Vries, P. S; Brown, M. R; Bentley, A. R; Sung, Y. J; Winkler, T. W; Ntalla, I.; Schwander, K.; Kraja, A. T; Guo, X.; Franceschini, N.; Cheng, C.; Sim, X.; Vojinovic, D.; Huffman, J. E; Musani, S. K; Li, C.; Feitosa, M. F; Richard, M. A; Noordam, R.; Aschard, H.; Bartz, T. M; Bielak, L. F; Deng, X.; Dorajoo, R.; Lohman, K. K; Manning, A. K; Rankinen, T.; Smith, A. V; Tajuddin, S. M; Evangelou, E.; Graff, M.; Alver, M.; Boissel, M.; Chai, J. F.; Chen, X.; Divers, J.; Gandin, I.; Gao, C.; Goel, A.; Hagemeijer, Y.; Harris, S. E; Hartwig, F. P; He, M.; Horimoto, A. R V R; Hsu, F.; Jackson, A. U; Kasturiratne, A.; Komulainen, P.; Kuhnel, B.; Laguzzi, F.; Lee, J. H; Luan, J.; Lyytikäinen, L.; Matoba, N.; Nolte, I. M; Pietzner, M.; Riaz, M.; Said, M A.; Scott, R. A; Sofer, T.; Stančáková, A.; Takeuchi, F.; Tayo, B. O; van der Most, P. J; Varga, T. V; Wang, Y.; Ware, E. B; Wen, W.; Yanek, L. R; Zhang, W.; Zhao, J. H.; Afaq, S.; Amin, N.; Amini, M.; Arking, D. E; Aung, T.; Ballantyne, C.; Boerwinkle, E.; Broeckel, U.; Campbell, A.; Canouil, M.; Charumathi, S.; Chen, Y. I.; Connell, J. M; de Faire, U.; de Las Fuentes, L.; de Mutsert, R.; de Silva, H J.; Ding, J.; Dominiczak, A. F; Duan, Q.; Eaton, C. B; Eppinga, R. N; Faul, J. D; Fisher, V.; Forrester, T.; Franco, O. H; Friedlander, Y.; Ghanbari, M.; Giulianini, F.; Grabe, H. J; Grove, M. L; Gu, C C.; Harris, T. B; Heikkinen, S.; Heng, C.; Hirata, M.; Hixson, J. E; Howard, B. V; Ikram, M A.; Jacobs, D. R; Johnson, C.; Jonas, J. B.; Kammerer, C. M; Katsuya, T.; Khor, C. C.; Kilpeläinen, T. O; Koh, W.; Koistinen, H. A; Kolcic, I.; Kooperberg, C.; Krieger, J. E; Kritchevsky, S. B; Kubo, M.; Kuusisto, J.; Lakka, T. A; Langefeld, C. D; Langenberg, C.; Launer, L. J; Lehne, B.; Lemaitre, R. N; Li, Y.; Liang, J.; Liu, J.; Liu, K.; Loh, M.; Louie, T.; Mägi, R.; Manichaikul, A. W; McKenzie, C. A; Meitinger, T.; Metspalu, A.; Milaneschi, Y.; Milani, L.; Mohlke, K. L; Mosley, T. H; Mukamal, K. J; Nalls, M. A; Nauck, M.; Nelson, C. P; Sotoodehnia, N.; O’Connell, J. R; Palmer, N. D; Pazoki, R.; Pedersen, N. L; Peters, A.; Peyser, P. A; Polasek, O.; Poulter, N.; Raffel, L. J; Raitakari, O. T; Reiner, A. P; Rice, T. K; Rich, S. S; Robino, A.; Robinson, J. G; Rose, L. M; Rudan, I.; Schmidt, C. O; Schreiner, P. J; Scott, W. R; Sever, P.; Shi, Y.; Sidney, S.; Sims, M.; Smith, B. H; Smith, J. A; Snieder, H.; Starr, J. M; Strauch, K.; Tan, N.; Taylor, K. D; Teo, Y. Y.; Tham, Y. C.; Uitterlinden, A. G; van Heemst, D.; Vuckovic, D.; Waldenberger, M.; Wang, L.; Wang, Y.; Wang, Z.; Wei, W. B.; Williams, C.; Wilson, G.; Wojczynski, M. K; Yao, J.; Yu, B.; Yu, C.; Yuan, J.; Zhao, W.; Zonderman, A. B; Becker, D. M; Boehnke, M.; Bowden, D. W; Chambers, J. C; Deary, I. J; Esko, T.; Farrall, M.; Franks, P. W; Freedman, B. I; Froguel, P.; Gasparini, P.; Gieger, C.; Horta, B. L; Kamatani, Y.; Kato, N.; Kooner, J. S; Laakso, M.; Leander, K.; Lehtimäki, T.; Magnusson, P. K E; Penninx, B.; Pereira, A. C; Rauramaa, R.; Samani, N. J; Scott, J.; Shu, X.; van der Harst, P.; Wagenknecht, L. E; Wang, Y. X.; Wareham, N. J; Watkins, H.; Weir, D. R; Wickremasinghe, A. R; Zheng, W.; Elliott, P.; North, K. E; Bouchard, C.; Evans, M. K; Gudnason, V.; Liu, C.; Liu, Y.; Psaty, B. M; Ridker, P. M; van Dam, R. M; Kardia, S. L R; Zhu, X.; Rotimi, C. N; Mook-Kanamori, D. O; Fornage, M.; Kelly, T. N; Fox, E. R; Hayward, C.; van Duijn, C. M; Tai, E S.; Wong, T. Y.; Liu, J.; Rotter, J. I; Gauderman, W J.; Province, M. A; Munroe, P. B; Rice, K.; Chasman, D. I; Cupples, L A.; Rao, D. C; and Morrison, A. C\n\n\n \n \n \n \n Multi-Ancestry Genome-Wide Association Study of Lipid Levels Incorporating Gene-Alcohol Interactions.\n \n \n \n\n\n \n\n\n\n Am J Epidemiol. January 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{de_vries_multi-ancestry_2019,\n\ttitle = {Multi-{Ancestry} {Genome}-{Wide} {Association} {Study} of {Lipid} {Levels} {Incorporating} {Gene}-{Alcohol} {Interactions}.},\n\tissn = {1476-6256},\n\tdoi = {10.1093/aje/kwz005},\n\tabstract = {{\\textless}p{\\textgreater}An individual’s lipid profile is influenced by genetic variants and alcohol consumption, but the contribution of interactions between these exposures has not been studied. We therefore incorporated gene-alcohol interactions into a multi-ancestry genome-wide association study of levels of high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglycerides. We included 45 studies in Stage 1 (genome-wide discovery) and 66 studies in Stage 2 (focused follow-up), for a total of 394,584 individuals from five ancestry groups. Genetic main and interaction effects were jointly assessed by a 2 degrees of freedom (DF) test, and a 1 DF test was used to assess the interaction effects alone. Variants at 495 loci were at least suggestively associated (P {\\textless} 1 × 10-6) with lipid levels in Stage 1 and were evaluated in Stage 2, followed by combined analyses of Stage 1 and Stage 2. In the combined analysis of Stage 1 and Stage 2, 147 independent loci were associated with lipid levels at P {\\textless} 5 × 10-8 using 2 DF tests, of which 18 were novel. No genome-wide significant associations were found testing the interaction effect alone. The novel loci included several genes (PCSK5, VEGFB, and A1CF) with a putative role in lipid metabolism based on existing evidence from cellular and experimental models.{\\textless}/p{\\textgreater}},\n\tjournal = {Am J Epidemiol},\n\tauthor = {de Vries, Paul S and Brown, Michael R and Bentley, Amy R and Sung, Yun J and Winkler, Thomas W and Ntalla, Ioanna and Schwander, Karen and Kraja, Aldi T and Guo, Xiuqing and Franceschini, Nora and Cheng, Ching-Yu and Sim, Xueling and Vojinovic, Dina and Huffman, Jennifer E and Musani, Solomon K and Li, Changwei and Feitosa, Mary F and Richard, Melissa A and Noordam, Raymond and Aschard, Hugues and Bartz, Traci M and Bielak, Lawrence F and Deng, Xuan and Dorajoo, Rajkumar and Lohman, Kurt K and Manning, Alisa K and Rankinen, Tuomo and Smith, Albert V and Tajuddin, Salman M and Evangelou, Evangelos and Graff, Mariaelisa and Alver, Maris and Boissel, Mathilde and Chai, Jin Fang and Chen, Xu and Divers, Jasmin and Gandin, Ilaria and Gao, Chuan and Goel, Anuj and Hagemeijer, Yanick and Harris, Sarah E and Hartwig, Fernando P and He, Meian and Horimoto, Andrea R V R and Hsu, Fang-Chi and Jackson, Anne U and Kasturiratne, Anuradhani and Komulainen, Pirjo and Kuhnel, Brigitte and Laguzzi, Federica and Lee, Joseph H and Luan, Jian’an and Lyytikäinen, Leo-Pekka and Matoba, Nana and Nolte, Ilja M and Pietzner, Maik and Riaz, Muhammad and Said, M Abdullah and Scott, Robert A and Sofer, Tamar and Stančáková, Alena and Takeuchi, Fumihiko and Tayo, Bamidele O and van der Most, Peter J and Varga, Tibor V and Wang, Yajuan and Ware, Erin B and Wen, Wanqing and Yanek, Lisa R and Zhang, Weihua and Zhao, Jing Hua and Afaq, Saima and Amin, Najaf and Amini, Marzyeh and Arking, Dan E and Aung, Tin and Ballantyne, Christie and Boerwinkle, Eric and Broeckel, Ulrich and Campbell, Archie and Canouil, Mickaël and Charumathi, Sabanayagam and Chen, Yii-Der Ida and Connell, John M and de Faire, Ulf and de Las Fuentes, Lisa and de Mutsert, Renée and de Silva, H Janaka and Ding, Jingzhong and Dominiczak, Anna F and Duan, Qing and Eaton, Charles B and Eppinga, Ruben N and Faul, Jessica D and Fisher, Virginia and Forrester, Terrence and Franco, Oscar H and Friedlander, Yechiel and Ghanbari, Mohsen and Giulianini, Franco and Grabe, Hans J and Grove, Megan L and Gu, C Charles and Harris, Tamara B and Heikkinen, Sami and Heng, Chew-Kiat and Hirata, Makoto and Hixson, James E and Howard, Barbara V and Ikram, M Arfan and Jacobs, David R and Johnson, Craig and Jonas, Jost Bruno and Kammerer, Candace M and Katsuya, Tomohiro and Khor, Chiea Chuen and Kilpeläinen, Tuomas O and Koh, Woon-Puay and Koistinen, Heikki A and Kolcic, Ivana and Kooperberg, Charles and Krieger, Jose E and Kritchevsky, Steve B and Kubo, Michiaki and Kuusisto, Johanna and Lakka, Timo A and Langefeld, Carl D and Langenberg, Claudia and Launer, Lenore J and Lehne, Benjamin and Lemaitre, Rozenn N and Li, Yize and Liang, Jingjing and Liu, Jianjun and Liu, Kiang and Loh, Marie and Louie, Tin and Mägi, Reedik and Manichaikul, Ani W and McKenzie, Colin A and Meitinger, Thomas and Metspalu, Andres and Milaneschi, Yuri and Milani, Lili and Mohlke, Karen L and Mosley, Thomas H and Mukamal, Kenneth J and Nalls, Mike A and Nauck, Matthias and Nelson, Christopher P and Sotoodehnia, Nona and O’Connell, Jeff R and Palmer, Nicholette D and Pazoki, Raha and Pedersen, Nancy L and Peters, Annette and Peyser, Patricia A and Polasek, Ozren and Poulter, Neil and Raffel, Leslie J and Raitakari, Olli T and Reiner, Alex P and Rice, Treva K and Rich, Stephen S and Robino, Antonietta and Robinson, Jennifer G and Rose, Lynda M and Rudan, Igor and Schmidt, Carsten O and Schreiner, Pamela J and Scott, William R and Sever, Peter and Shi, Yuan and Sidney, Stephen and Sims, Mario and Smith, Blair H and Smith, Jennifer A and Snieder, Harold and Starr, John M and Strauch, Konstantin and Tan, Nicholas and Taylor, Kent D and Teo, Yik Ying and Tham, Yih Chung and Uitterlinden, André G and van Heemst, Diana and Vuckovic, Dragana and Waldenberger, Melanie and Wang, Lihua and Wang, Yujie and Wang, Zhe and Wei, Wen Bin and Williams, Christine and Wilson, Gregory and Wojczynski, Mary K and Yao, Jie and Yu, Bing and Yu, Caizheng and Yuan, Jian-Min and Zhao, Wei and Zonderman, Alan B and Becker, Diane M and Boehnke, Michael and Bowden, Donald W and Chambers, John C and Deary, Ian J and Esko, Tõnu and Farrall, Martin and Franks, Paul W and Freedman, Barry I and Froguel, Philippe and Gasparini, Paolo and Gieger, Christian and Horta, Bernardo L and Kamatani, Yoichiro and Kato, Norihiro and Kooner, Jaspal S and Laakso, Markku and Leander, Karin and Lehtimäki, Terho and Magnusson, Patrik K E and Penninx, Brenda and Pereira, Alexandre C and Rauramaa, Rainer and Samani, Nilesh J and Scott, James and Shu, Xiao-Ou and van der Harst, Pim and Wagenknecht, Lynne E and Wang, Ya Xing and Wareham, Nicholas J and Watkins, Hugh and Weir, David R and Wickremasinghe, Ananda R and Zheng, Wei and Elliott, Paul and North, Kari E and Bouchard, Claude and Evans, Michele K and Gudnason, Vilmundur and Liu, Ching-Ti and Liu, Yongmei and Psaty, Bruce M and Ridker, Paul M and van Dam, Rob M and Kardia, Sharon L R and Zhu, Xiaofeng and Rotimi, Charles N and Mook-Kanamori, Dennis O and Fornage, Myriam and Kelly, Tanika N and Fox, Ervin R and Hayward, Caroline and van Duijn, Cornelia M and Tai, E Shyong and Wong, Tien Yin and Liu, Jingmin and Rotter, Jerome I and Gauderman, W James and Province, Michael A and Munroe, Patricia B and Rice, Kenneth and Chasman, Daniel I and Cupples, L Adrienne and Rao, Dabeeru C and Morrison, Alanna C},\n\tmonth = jan,\n\tyear = {2019},\n}\n\n\n\n

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\n \n\n \n \n Ward-Caviness, C. K; de Vries, P. S; Wiggins, K. L; Huffman, J. E; Yanek, L. R; Bielak, L. F; Giulianini, F.; Guo, X.; Kleber, M. E; Kacprowski, T.; Groß, S.; Petersman, A.; Davey Smith, G.; Hartwig, F. P; Bowden, J.; Hemani, G.; Müller-Nuraysid, M.; Strauch, K.; Koenig, W.; Waldenberger, M.; Meitinger, T.; Pankratz, N.; Boerwinkle, E.; Tang, W.; Fu, Y.; Johnson, A. D; Song, C.; de Maat, M. P M; Uitterlinden, A. G; Franco, O. H; Brody, J. A; McKnight, B.; Chen, Y. I.; Psaty, B. M; Mathias, R. A; Becker, D. M; Peyser, P. A; Smith, J. A; Bielinski, S. J; Ridker, P. M; Taylor, K. D; Yao, J.; Tracy, R.; Delgado, G.; Trompet, S.; Sattar, N.; Jukema, J W.; Becker, L. C; Kardia, S. L R; Rotter, J. I; März, W.; Dörr, M.; Chasman, D. I; Dehghan, A.; O’Donnell, C. J; Smith, N. L; Peters, A.; and Morrison, A. C\n\n\n \n \n \n \n Mendelian randomization evaluation of causal effects of fibrinogen on incident coronary heart disease.\n \n \n \n\n\n \n\n\n\n PLoS One, 14: e0216222. 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{ward-caviness_mendelian_2019,\n\ttitle = {Mendelian randomization evaluation of causal effects of fibrinogen on incident coronary heart disease.},\n\tvolume = {14},\n\tissn = {1932-6203},\n\tdoi = {10.1371/journal.pone.0216222},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{BACKGROUND: }Fibrinogen is an essential hemostatic factor and cardiovascular disease risk factor. Early attempts at evaluating the causal effect of fibrinogen on coronary heart disease (CHD) and myocardial infraction (MI) using Mendelian randomization (MR) used single variant approaches, and did not take advantage of recent genome-wide association studies (GWAS) or multi-variant, pleiotropy robust MR methodologies.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS AND FINDINGS: }We evaluated evidence for a causal effect of fibrinogen on both CHD and MI using MR. We used both an allele score approach and pleiotropy robust MR models. The allele score was composed of 38 fibrinogen-associated variants from recent GWAS. Initial analyses using the allele score used a meta-analysis of 11 European-ancestry prospective cohorts, free of CHD and MI at baseline, to examine incidence CHD and MI. We also applied 2 sample MR methods with data from a prevalent CHD and MI GWAS. Results are given in terms of the hazard ratio (HR) or odds ratio (OR), depending on the study design, and associated 95\\% confidence interval (CI). In single variant analyses no causal effect of fibrinogen on CHD or MI was observed. In multi-variant analyses using incidence CHD cases and the allele score approach, the estimated causal effect (HR) of a 1 g/L higher fibrinogen concentration was 1.62 (CI = 1.12, 2.36) when using incident cases and the allele score approach. In 2 sample MR analyses that accounted for pleiotropy, the causal estimate (OR) was reduced to 1.18 (CI = 0.98, 1.42) and 1.09 (CI = 0.89, 1.33) in the 2 most precise (smallest CI) models, out of 4 models evaluated. In the 2 sample MR analyses for MI, there was only very weak evidence of a causal effect in only 1 out of 4 models.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSIONS: }A small causal effect of fibrinogen on CHD is observed using multi-variant MR approaches which account for pleiotropy, but not single variant MR approaches. Taken together, results indicate that even with large sample sizes and multi-variant approaches MR analyses still cannot exclude the null when estimating the causal effect of fibrinogen on CHD, but that any potential causal effect is likely to be much smaller than observed in epidemiological studies.{\\textless}/p{\\textgreater}},\n\tjournal = {PLoS One},\n\tauthor = {Ward-Caviness, Cavin K and de Vries, Paul S and Wiggins, Kerri L and Huffman, Jennifer E and Yanek, Lisa R and Bielak, Lawrence F and Giulianini, Franco and Guo, Xiuqing and Kleber, Marcus E and Kacprowski, Tim and Groß, Stefan and Petersman, Astrid and Davey Smith, George and Hartwig, Fernando P and Bowden, Jack and Hemani, Gibran and Müller-Nuraysid, Martina and Strauch, Konstantin and Koenig, Wolfgang and Waldenberger, Melanie and Meitinger, Thomas and Pankratz, Nathan and Boerwinkle, Eric and Tang, Weihong and Fu, Yi-Ping and Johnson, Andrew D and Song, Ci and de Maat, Moniek P M and Uitterlinden, André G and Franco, Oscar H and Brody, Jennifer A and McKnight, Barbara and Chen, Yii-Der Ida and Psaty, Bruce M and Mathias, Rasika A and Becker, Diane M and Peyser, Patricia A and Smith, Jennifer A and Bielinski, Suzette J and Ridker, Paul M and Taylor, Kent D and Yao, Jie and Tracy, Russell and Delgado, Graciela and Trompet, Stella and Sattar, Naveed and Jukema, J Wouter and Becker, Lewis C and Kardia, Sharon L R and Rotter, Jerome I and März, Winfried and Dörr, Marcus and Chasman, Daniel I and Dehghan, Abbas and O’Donnell, Christopher J and Smith, Nicholas L and Peters, Annette and Morrison, Alanna C},\n\tyear = {2019},\n\tpages = {e0216222},\n}\n\n\n\n

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\n \\textlessp\\textgreater\\textbfBACKGROUND: Fibrinogen is an essential hemostatic factor and cardiovascular disease risk factor. Early attempts at evaluating the causal effect of fibrinogen on coronary heart disease (CHD) and myocardial infraction (MI) using Mendelian randomization (MR) used single variant approaches, and did not take advantage of recent genome-wide association studies (GWAS) or multi-variant, pleiotropy robust MR methodologies.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfMETHODS AND FINDINGS: We evaluated evidence for a causal effect of fibrinogen on both CHD and MI using MR. We used both an allele score approach and pleiotropy robust MR models. The allele score was composed of 38 fibrinogen-associated variants from recent GWAS. Initial analyses using the allele score used a meta-analysis of 11 European-ancestry prospective cohorts, free of CHD and MI at baseline, to examine incidence CHD and MI. We also applied 2 sample MR methods with data from a prevalent CHD and MI GWAS. Results are given in terms of the hazard ratio (HR) or odds ratio (OR), depending on the study design, and associated 95% confidence interval (CI). In single variant analyses no causal effect of fibrinogen on CHD or MI was observed. In multi-variant analyses using incidence CHD cases and the allele score approach, the estimated causal effect (HR) of a 1 g/L higher fibrinogen concentration was 1.62 (CI = 1.12, 2.36) when using incident cases and the allele score approach. In 2 sample MR analyses that accounted for pleiotropy, the causal estimate (OR) was reduced to 1.18 (CI = 0.98, 1.42) and 1.09 (CI = 0.89, 1.33) in the 2 most precise (smallest CI) models, out of 4 models evaluated. In the 2 sample MR analyses for MI, there was only very weak evidence of a causal effect in only 1 out of 4 models.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfCONCLUSIONS: A small causal effect of fibrinogen on CHD is observed using multi-variant MR approaches which account for pleiotropy, but not single variant MR approaches. Taken together, results indicate that even with large sample sizes and multi-variant approaches MR analyses still cannot exclude the null when estimating the causal effect of fibrinogen on CHD, but that any potential causal effect is likely to be much smaller than observed in epidemiological studies.\\textless/p\\textgreater\n

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\n \n\n \n \n Sarnowski, C.; Leong, A.; Raffield, L. M; Wu, P.; de Vries, P. S; DiCorpo, D.; Guo, X.; Xu, H.; Liu, Y.; Zheng, X.; Hu, Y.; Brody, J. A; Goodarzi, M. O; Hidalgo, B. A; Highland, H. M; Jain, D.; Liu, C.; Naik, R. P; O’Connell, J. R; Perry, J. A; Porneala, B. C; Selvin, E.; Wessel, J.; Psaty, B. M; Curran, J. E; Peralta, J. M; Blangero, J.; Kooperberg, C.; Mathias, R.; Johnson, A. D; Reiner, A. P; Mitchell, B. D; Cupples, L A.; Vasan, R. S; Correa, A.; Morrison, A. C; Boerwinkle, E.; Rotter, J. I; Rich, S. S; Manning, A. K; Dupuis, J.; and Meigs, J. B\n\n\n \n \n \n \n Impact of Rare and Common Genetic Variants on Diabetes Diagnosis by Hemoglobin A1c in Multi-Ancestry Cohorts: The Trans-Omics for Precision Medicine Program.\n \n \n \n\n\n \n\n\n\n Am J Hum Genet, 105: 706–718. October 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{sarnowski_impact_2019,\n\ttitle = {Impact of {Rare} and {Common} {Genetic} {Variants} on {Diabetes} {Diagnosis} by {Hemoglobin} {A1c} in {Multi}-{Ancestry} {Cohorts}: {The} {Trans}-{Omics} for {Precision} {Medicine} {Program}.},\n\tvolume = {105},\n\tissn = {1537-6605},\n\tdoi = {10.1016/j.ajhg.2019.08.010},\n\tabstract = {{\\textless}p{\\textgreater}Hemoglobin A1c (HbA1c) is widely used to diagnose diabetes and assess glycemic control in individuals with diabetes. However, nonglycemic determinants, including genetic variation, may influence how accurately HbA1c reflects underlying glycemia. Analyzing the NHLBI Trans-Omics for Precision Medicine (TOPMed) sequence data in 10,338 individuals from five studies and four ancestries (6,158 Europeans, 3,123 African-Americans, 650 Hispanics, and 407 East Asians), we confirmed five regions associated with HbA1c (GCK in Europeans and African-Americans, HK1 in Europeans and Hispanics, FN3K and/or FN3KRP in Europeans, and G6PD in African-Americans and Hispanics) and we identified an African-ancestry-specific low-frequency variant (rs1039215 in HBG2 and HBE1, minor allele frequency (MAF) = 0.03). The most associated G6PD variant (rs1050828-T, p.Val98Met, MAF = 12\\% in African-Americans, MAF = 2\\% in Hispanics) lowered HbA1c (-0.88\\% in hemizygous males, -0.34\\% in heterozygous females) and explained 23\\% of HbA1c variance in African-Americans and 4\\% in Hispanics. Additionally, we identified a rare distinct G6PD coding variant (rs76723693, p.Leu353Pro, MAF = 0.5\\%; -0.98\\% in hemizygous males, -0.46\\% in heterozygous females) and detected significant association with HbA1c when aggregating rare missense variants in G6PD. We observed similar magnitude and direction of effects for rs1039215 (HBG2) and rs76723693 (G6PD) in the two largest TOPMed African American cohorts, and we replicated the rs76723693 association in the UK Biobank African-ancestry participants. These variants in G6PD and HBG2 were monomorphic in the European and Asian samples. African or Hispanic ancestry individuals carrying G6PD variants may be underdiagnosed for diabetes when screened with HbA1c. Thus, assessment of these variants should be considered for incorporation into precision medicine approaches for diabetes diagnosis.{\\textless}/p{\\textgreater}},\n\tjournal = {Am J Hum Genet},\n\tauthor = {Sarnowski, Chloe and Leong, Aaron and Raffield, Laura M and Wu, Peitao and de Vries, Paul S and DiCorpo, Daniel and Guo, Xiuqing and Xu, Huichun and Liu, Yongmei and Zheng, Xiuwen and Hu, Yao and Brody, Jennifer A and Goodarzi, Mark O and Hidalgo, Bertha A and Highland, Heather M and Jain, Deepti and Liu, Ching-Ti and Naik, Rakhi P and O’Connell, Jeffrey R and Perry, James A and Porneala, Bianca C and Selvin, Elizabeth and Wessel, Jennifer and Psaty, Bruce M and Curran, Joanne E and Peralta, Juan M and Blangero, John and Kooperberg, Charles and Mathias, Rasika and Johnson, Andrew D and Reiner, Alexander P and Mitchell, Braxton D and Cupples, L Adrienne and Vasan, Ramachandran S and Correa, Adolfo and Morrison, Alanna C and Boerwinkle, Eric and Rotter, Jerome I and Rich, Stephen S and Manning, Alisa K and Dupuis, Josée and Meigs, James B},\n\tmonth = oct,\n\tyear = {2019},\n\tpages = {706--718},\n}\n\n\n\n

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\n \n\n \n \n Adhikari, S.; Lecci, F.; Becker, J. T; Junker, B. W; Kuller, L. H; Lopez, O. L; and Tibshirani, R. J\n\n\n \n \n \n \n High-dimensional longitudinal classification with the multinomial fused lasso.\n \n \n \n\n\n \n\n\n\n Stat Med. January 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{adhikari_high-dimensional_2019,\n\ttitle = {High-dimensional longitudinal classification with the multinomial fused lasso.},\n\tissn = {1097-0258},\n\tdoi = {10.1002/sim.8100},\n\tabstract = {{\\textless}p{\\textgreater}We study regularized estimation in high-dimensional longitudinal classification problems, using the lasso and fused lasso regularizers. The constructed coefficient estimates are piecewise constant across the time dimension in the longitudinal problem, with adaptively selected change points (break points). We present an efficient algorithm for computing such estimates, based on proximal gradient descent. We apply our proposed technique to a longitudinal data set on Alzheimer’s disease from the Cardiovascular Health Study Cognition Study. Using data analysis and a simulation study, we motivate and demonstrate several practical considerations such as the selection of tuning parameters and the assessment of model stability. While race, gender, vascular and heart disease, lack of caregivers, and deterioration of learning and memory are all important predictors of dementia, we also find that these risk factors become more relevant in the later stages of life.{\\textless}/p{\\textgreater}},\n\tjournal = {Stat Med},\n\tauthor = {Adhikari, Samrachana and Lecci, Fabrizio and Becker, James T and Junker, Brian W and Kuller, Lewis H and Lopez, Oscar L and Tibshirani, Ryan J},\n\tmonth = jan,\n\tyear = {2019},\n}\n\n\n\n

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\n \n\n \n \n Timmers, P. R.; Mounier, N.; Läll, K.; Fischer, K.; Ning, Z.; Feng, X.; Bretherick, A. D; Clark, D. W; Agbessi, M; Ahsan, H; Alves, I; Andiappan, A; Awadalla, P; Battle, A; Bonder, M J; Boomsma, D; Christiansen, M; Claringbould, A; Deelen, P; van Dongen, J; Esko, T; Favé, M; Franke, L; Frayling, T; Gharib, S A; Gibson, G; Hemani, G; Jansen, R; Kalnapenkis, A; Kasela, S; Kettunen, J; Kim, Y; Kirsten, H; Kovacs, P; Krohn, K; Kronberg-Guzman, J; Kukushkina, V; Kutalik, Z; Kähönen, M; Lee, B; Lehtimäki, T; Loeffler, M; Marigorta, U; Metspalu, A; van Meurs, J; Milani, L; Müller-Nurasyid, M; Nauck, M; Nivard, M; Penninx, B; Perola, M; Pervjakova, N; Pierce, B; Powell, J; Prokisch, H; Psaty, B M; Raitakari, O; Ring, S; Ripatti, S; Rotzschke, O; Ruëger, S; Saha, A; Scholz, M; Schramm, K; Seppälä, I; Stumvoll, M; Sullivan, P; Teumer, A; Thiery, J; Tong, L; Tönjes, A; Verlouw, J; Visscher, P M; Võsa, U; Völker, U; Yaghootkar, H; Yang, J; Zeng, B; Zhang, F; Agbessi, M; Ahsan, H; Alves, I; Andiappan, A; Awadalla, P; Battle, A; Bonder, M J; Boomsma, D; Christiansen, M; Claringbould, A; Deelen, P; van Dongen, J; Esko, T; Favé, M; Franke, L; Frayling, T; Gharib, S A; Gibson, G; Hemani, G; Jansen, R; Kalnapenkis, A; Kasela, S; Kettunen, J; Kim, Y; Kirsten, H; Kovacs, P; Krohn, K; Kronberg-Guzman, J; Kukushkina, V; Kutalik, Z; Kähönen, M; Lee, B; Lehtimäki, T; Loeffler, M; Marigorta, U; Metspalu, A; van Meurs, J; Milani, L; Müller-Nurasyid, M; Nauck, M; Nivard, M; Penninx, B; Perola, M; Pervjakova, N; Pierce, B; Powell, J; Prokisch, H; Psaty, B M; Raitakari, O; Ring, S; Ripatti, S; Rotzschke, O; Ruëger, S; Saha, A; Scholz, M; Schramm, K; Seppälä, I; Stumvoll, M; Sullivan, P; Teumer, A; Thiery, J; Tong, L; Tönjes, A; Verlouw, J; Visscher, P M; Võsa, U; Völker, U; Yaghootkar, H; Yang, J; Zeng, B; Zhang, F; Shen, X.; Esko, T.; Kutalik, Z.; Wilson, J. F; and Joshi, P. K\n\n\n \n \n \n \n Genomics of 1 million parent lifespans implicates novel pathways and common diseases and distinguishes survival chances.\n \n \n \n\n\n \n\n\n\n Elife, 8. January 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{timmers_genomics_2019,\n\ttitle = {Genomics of 1 million parent lifespans implicates novel pathways and common diseases and distinguishes survival chances.},\n\tvolume = {8},\n\tissn = {2050-084X},\n\tdoi = {10.7554/eLife.39856},\n\tabstract = {{\\textless}p{\\textgreater}We use a genome-wide association of 1 million parental lifespans of genotyped subjects and data on mortality risk factors to validate previously unreplicated findings near , , , , , and 13q21.31, and identify and replicate novel findings near , , and . We also validate previous findings near 5q33.3/ and , whilst finding contradictory evidence at other loci. Gene set and cell-specific analyses show that expression in foetal brain cells and adult dorsolateral prefrontal cortex is enriched for lifespan variation, as are gene pathways involving lipid proteins and homeostasis, vesicle-mediated transport, and synaptic function. Individual genetic variants that increase dementia, cardiovascular disease, and lung cancer - but not other cancers - explain the most variance. Resulting polygenic scores show a mean lifespan difference of around five years of life across the deciles.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{Editorial note: }This article has been through an editorial process in which the authors decide how to respond to the issues raised during peer review. The Reviewing Editor’s assessment is that all the issues have been addressed (see decision letter).{\\textless}/p{\\textgreater}},\n\tjournal = {Elife},\n\tauthor = {Timmers, Paul Rhj and Mounier, Ninon and Läll, Kristi and Fischer, Krista and Ning, Zheng and Feng, Xiao and Bretherick, Andrew D and Clark, David W and Agbessi, M and Ahsan, H and Alves, I and Andiappan, A and Awadalla, P and Battle, A and Bonder, M J and Boomsma, D and Christiansen, M and Claringbould, A and Deelen, P and van Dongen, J and Esko, T and Favé, M and Franke, L and Frayling, T and Gharib, S A and Gibson, G and Hemani, G and Jansen, R and Kalnapenkis, A and Kasela, S and Kettunen, J and Kim, Y and Kirsten, H and Kovacs, P and Krohn, K and Kronberg-Guzman, J and Kukushkina, V and Kutalik, Z and Kähönen, M and Lee, B and Lehtimäki, T and Loeffler, M and Marigorta, U and Metspalu, A and van Meurs, J and Milani, L and Müller-Nurasyid, M and Nauck, M and Nivard, M and Penninx, B and Perola, M and Pervjakova, N and Pierce, B and Powell, J and Prokisch, H and Psaty, B M and Raitakari, O and Ring, S and Ripatti, S and Rotzschke, O and Ruëger, S and Saha, A and Scholz, M and Schramm, K and Seppälä, I and Stumvoll, M and Sullivan, P and Teumer, A and Thiery, J and Tong, L and Tönjes, A and Verlouw, J and Visscher, P M and Võsa, U and Völker, U and Yaghootkar, H and Yang, J and Zeng, B and Zhang, F and Agbessi, M and Ahsan, H and Alves, I and Andiappan, A and Awadalla, P and Battle, A and Bonder, M J and Boomsma, D and Christiansen, M and Claringbould, A and Deelen, P and van Dongen, J and Esko, T and Favé, M and Franke, L and Frayling, T and Gharib, S A and Gibson, G and Hemani, G and Jansen, R and Kalnapenkis, A and Kasela, S and Kettunen, J and Kim, Y and Kirsten, H and Kovacs, P and Krohn, K and Kronberg-Guzman, J and Kukushkina, V and Kutalik, Z and Kähönen, M and Lee, B and Lehtimäki, T and Loeffler, M and Marigorta, U and Metspalu, A and van Meurs, J and Milani, L and Müller-Nurasyid, M and Nauck, M and Nivard, M and Penninx, B and Perola, M and Pervjakova, N and Pierce, B and Powell, J and Prokisch, H and Psaty, B M and Raitakari, O and Ring, S and Ripatti, S and Rotzschke, O and Ruëger, S and Saha, A and Scholz, M and Schramm, K and Seppälä, I and Stumvoll, M and Sullivan, P and Teumer, A and Thiery, J and Tong, L and Tönjes, A and Verlouw, J and Visscher, P M and Võsa, U and Völker, U and Yaghootkar, H and Yang, J and Zeng, B and Zhang, F and Shen, Xia and Esko, Tõnu and Kutalik, Zoltán and Wilson, James F and Joshi, Peter K},\n\tmonth = jan,\n\tyear = {2019},\n}\n\n\n\n

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\n \n\n \n \n Lindström, S.; Wang, L.; Smith, E. N; Gordon, W.; van Hylckama Vlieg, A.; de Andrade, M.; Brody, J. A; Pattee, J. W; Haessler, J.; Brumpton, B. M; Chasman, D. I; Suchon, P.; Chen, M.; Turman, C.; Germain, M.; Wiggins, K. L; MacDonald, J.; Braekkan, S. K; Armasu, S. M; Pankratz, N.; Jackson, R. D; Nielsen, J. B; Giulianini, F.; Puurunen, M. K; Ibrahim, M.; Heckbert, S. R; Damrauer, S. M; Natarajan, P.; Klarin, D.; de Vries, P. S; Sabater-Lleal, M.; Huffman, J. E; Bammler, T. K; Frazer, K. A; McCauley, B. M; Taylor, K.; Pankow, J. S; Reiner, A. P; Gabrielsen, M. E; Deleuze, J.; O’Donnell, C. J; Kim, J.; McKnight, B.; Kraft, P.; Hansen, J.; Rosendaal, F. R; Heit, J. A; Psaty, B. M; Tang, W.; Kooperberg, C.; Hveem, K.; Ridker, P. M; Morange, P.; Johnson, A. D; Kabrhel, C.; Trégouët, D.; and Smith, N. L\n\n\n \n \n \n \n Genomic and transcriptomic association studies identify 16 novel susceptibility loci for venous thromboembolism.\n \n \n \n\n\n \n\n\n\n Blood, 134: 1645–1657. November 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{lindstrom_genomic_2019,\n\ttitle = {Genomic and transcriptomic association studies identify 16 novel susceptibility loci for venous thromboembolism.},\n\tvolume = {134},\n\tissn = {1528-0020},\n\tdoi = {10.1182/blood.2019000435},\n\tabstract = {{\\textless}p{\\textgreater}Venous thromboembolism (VTE) is a significant contributor to morbidity and mortality. To advance our understanding of the biology contributing to VTE, we conducted a genome-wide association study (GWAS) of VTE and a transcriptome-wide association study (TWAS) based on imputed gene expression from whole blood and liver. We meta-analyzed GWAS data from 18 studies for 30 234 VTE cases and 172 122 controls and assessed the association between 12 923 718 genetic variants and VTE. We generated variant prediction scores of gene expression from whole blood and liver tissue and assessed them for association with VTE. Mendelian randomization analyses were conducted for traits genetically associated with novel VTE loci. We identified 34 independent genetic signals for VTE risk from GWAS meta-analysis, of which 14 are newly reported associations. This included 11 newly associated genetic loci (C1orf198, PLEK, OSMR-AS1, NUGGC/SCARA5, GRK5, MPHOSPH9, ARID4A, PLCG2, SMG6, EIF5A, and STX10) of which 6 replicated, and 3 new independent signals in 3 known genes. Further, TWAS identified 5 additional genetic loci with imputed gene expression levels differing between cases and controls in whole blood (SH2B3, SPSB1, RP11-747H7.3, RP4-737E23.2) and in liver (ERAP1). At some GWAS loci, we found suggestive evidence that the VTE association signal for novel and previously known regions colocalized with expression quantitative trait locus signals. Mendelian randomization analyses suggested that blood traits may contribute to the underlying risk of VTE. To conclude, we identified 16 novel susceptibility loci for VTE; for some loci, the association signals are likely mediated through gene expression of nearby genes.{\\textless}/p{\\textgreater}},\n\tjournal = {Blood},\n\tauthor = {Lindström, Sara and Wang, Lu and Smith, Erin N and Gordon, William and van Hylckama Vlieg, Astrid and de Andrade, Mariza and Brody, Jennifer A and Pattee, Jack W and Haessler, Jeffrey and Brumpton, Ben M and Chasman, Daniel I and Suchon, Pierre and Chen, Ming-Huei and Turman, Constance and Germain, Marine and Wiggins, Kerri L and MacDonald, James and Braekkan, Sigrid K and Armasu, Sebastian M and Pankratz, Nathan and Jackson, Rebecca D and Nielsen, Jonas B and Giulianini, Franco and Puurunen, Marja K and Ibrahim, Manal and Heckbert, Susan R and Damrauer, Scott M and Natarajan, Pradeep and Klarin, Derek and de Vries, Paul S and Sabater-Lleal, Maria and Huffman, Jennifer E and Bammler, Theo K and Frazer, Kelly A and McCauley, Bryan M and Taylor, Kent and Pankow, James S and Reiner, Alexander P and Gabrielsen, Maiken E and Deleuze, Jean-Francois and O’Donnell, Chris J and Kim, Jihye and McKnight, Barbara and Kraft, Peter and Hansen, John-Bjarne and Rosendaal, Frits R and Heit, John A and Psaty, Bruce M and Tang, Weihong and Kooperberg, Charles and Hveem, Kristian and Ridker, Paul M and Morange, Pierre-Emmanuel and Johnson, Andrew D and Kabrhel, Christopher and Trégouët, David-Alexandre and Smith, Nicholas L},\n\tmonth = nov,\n\tyear = {2019},\n\tpages = {1645--1657},\n}\n\n\n\n

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\n \n\n \n \n Dashti, H. S; Merino, J.; Lane, J. M; Song, Y.; Smith, C. E; Tanaka, T.; McKeown, N. M; Tucker, C.; Sun, D.; Bartz, T. M; Li-Gao, R.; Nisa, H.; Reutrakul, S.; Lemaitre, R. N; Alshehri, T. M; de Mutsert, R.; Bazzano, L.; Qi, L.; Knutson, K. L; Psaty, B. M; Mook-Kanamori, D. O; Perica, V. B.; Neuhouser, M. L; Scheer, F. A J L; Rutter, M. K; Garaulet, M.; and Saxena, R.\n\n\n \n \n \n \n Genome-wide association study of breakfast skipping links clock regulation with food timing.\n \n \n \n\n\n \n\n\n\n Am J Clin Nutr. June 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{dashti_genome-wide_2019,\n\ttitle = {Genome-wide association study of breakfast skipping links clock regulation with food timing.},\n\tissn = {1938-3207},\n\tdoi = {10.1093/ajcn/nqz076},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{BACKGROUND: }Little is known about the contribution of genetic variation to food timing, and breakfast has been determined to exhibit the most heritable meal timing. As breakfast timing and skipping are not routinely measured in large cohort studies, alternative approaches include analyses of correlated traits.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{OBJECTIVES: }The aim of this study was to elucidate breakfast skipping genetic variants through a proxy-phenotype genome-wide association study (GWAS) for breakfast cereal skipping, a commonly assessed correlated trait.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS: }We leveraged the statistical power of the UK Biobank (n = 193,860) to identify genetic variants related to breakfast cereal skipping as a proxy-phenotype for breakfast skipping and applied several in silico approaches to investigate mechanistic functions and links to traits/diseases. Next, we attempted validation of our approach in smaller breakfast skipping GWAS from the TwinUK (n = 2,006) and the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium (n = 11,963).{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{RESULTS: }In the UK Biobank, we identified 6 independent GWAS variants, including those implicated for caffeine (ARID3B/CYP1A1), carbohydrate metabolism (FGF21), schizophrenia (ZNF804A), and encoding enzymes important for N6-methyladenosine RNA transmethylation (METTL4, YWHAB, and YTHDF3), which regulates the pace of the circadian clock. Expression of identified genes was enriched in the cerebellum. Genome-wide correlation analyses indicated positive correlations with anthropometric traits. Through Mendelian randomization (MR), we observed causal links between genetically determined breakfast skipping and higher body mass index, more depressive symptoms, and smoking. In bidirectional MR, we demonstrated a causal link between being an evening person and skipping breakfast, but not vice versa. We observed association of our signals in an independent breakfast skipping GWAS in another British cohort (P = 0.032), TwinUK, but not in a meta-analysis of non-British cohorts from the CHARGE consortium (P = 0.095).{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSIONS: }Our proxy-phenotype GWAS identified 6 genetic variants for breakfast skipping, linking clock regulation with food timing and suggesting a possible beneficial role of regular breakfast intake as part of a healthy lifestyle.{\\textless}/p{\\textgreater}},\n\tjournal = {Am J Clin Nutr},\n\tauthor = {Dashti, Hassan S and Merino, Jordi and Lane, Jacqueline M and Song, Yanwei and Smith, Caren E and Tanaka, Toshiko and McKeown, Nicola M and Tucker, Chandler and Sun, Dianjianyi and Bartz, Traci M and Li-Gao, Ruifang and Nisa, Hoirun and Reutrakul, Sirimon and Lemaitre, Rozenn N and Alshehri, Tahani M and de Mutsert, Renée and Bazzano, Lydia and Qi, Lu and Knutson, Kristen L and Psaty, Bruce M and Mook-Kanamori, Dennis O and Perica, Vesna Boraska and Neuhouser, Marian L and Scheer, Frank A J L and Rutter, Martin K and Garaulet, Marta and Saxena, Richa},\n\tmonth = jun,\n\tyear = {2019},\n}\n\n\n\n

\n\n\n

\n \\textlessp\\textgreater\\textbfBACKGROUND: Little is known about the contribution of genetic variation to food timing, and breakfast has been determined to exhibit the most heritable meal timing. As breakfast timing and skipping are not routinely measured in large cohort studies, alternative approaches include analyses of correlated traits.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfOBJECTIVES: The aim of this study was to elucidate breakfast skipping genetic variants through a proxy-phenotype genome-wide association study (GWAS) for breakfast cereal skipping, a commonly assessed correlated trait.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfMETHODS: We leveraged the statistical power of the UK Biobank (n = 193,860) to identify genetic variants related to breakfast cereal skipping as a proxy-phenotype for breakfast skipping and applied several in silico approaches to investigate mechanistic functions and links to traits/diseases. Next, we attempted validation of our approach in smaller breakfast skipping GWAS from the TwinUK (n = 2,006) and the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium (n = 11,963).\\textless/p\\textgreater\\textlessp\\textgreater\\textbfRESULTS: In the UK Biobank, we identified 6 independent GWAS variants, including those implicated for caffeine (ARID3B/CYP1A1), carbohydrate metabolism (FGF21), schizophrenia (ZNF804A), and encoding enzymes important for N6-methyladenosine RNA transmethylation (METTL4, YWHAB, and YTHDF3), which regulates the pace of the circadian clock. Expression of identified genes was enriched in the cerebellum. Genome-wide correlation analyses indicated positive correlations with anthropometric traits. Through Mendelian randomization (MR), we observed causal links between genetically determined breakfast skipping and higher body mass index, more depressive symptoms, and smoking. In bidirectional MR, we demonstrated a causal link between being an evening person and skipping breakfast, but not vice versa. We observed association of our signals in an independent breakfast skipping GWAS in another British cohort (P = 0.032), TwinUK, but not in a meta-analysis of non-British cohorts from the CHARGE consortium (P = 0.095).\\textless/p\\textgreater\\textlessp\\textgreater\\textbfCONCLUSIONS: Our proxy-phenotype GWAS identified 6 genetic variants for breakfast skipping, linking clock regulation with food timing and suggesting a possible beneficial role of regular breakfast intake as part of a healthy lifestyle.\\textless/p\\textgreater\n

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\n \n\n \n \n de Vries, P. S; Sabater-Lleal, M.; Huffman, J. E; Marten, J.; Song, C.; Pankratz, N.; Bartz, T. M; de Haan, H. G; Delgado, G. E; Eicher, J. D; Martinez-Perez, A.; Ward-Caviness, C. K; Brody, J. A; Chen, M.; de Maat, M. P M; Frånberg, M.; Gill, D.; Kleber, M. E; Rivadeneira, F.; Soria, J. M.; Tang, W.; Tofler, G. H; Uitterlinden, A. G; van Hylckama Vlieg, A.; Seshadri, S.; Boerwinkle, E.; Davies, N. M; Giese, A.; Ikram, M K.; Kittner, S. J; McKnight, B.; Psaty, B. M; Reiner, A. P; Sargurupremraj, M.; Taylor, K. D; Fornage, M.; Hamsten, A.; März, W.; Rosendaal, F. R; Souto, J. C.; Dehghan, A.; Johnson, A. D; Morrison, A. C; O’Donnell, C. J; and Smith, N. L\n\n\n \n \n \n \n A genome-wide association study identifies new loci for factor VII and implicates factor VII in ischemic stroke etiology.\n \n \n \n\n\n \n\n\n\n Blood, 133: 967–977. February 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{de_vries_genome-wide_2019,\n\ttitle = {A genome-wide association study identifies new loci for factor {VII} and implicates factor {VII} in ischemic stroke etiology.},\n\tvolume = {133},\n\tissn = {1528-0020},\n\tdoi = {10.1182/blood-2018-05-849240},\n\tabstract = {{\\textless}p{\\textgreater}Factor VII (FVII) is an important component of the coagulation cascade. Few genetic loci regulating FVII activity and/or levels have been discovered to date. We conducted a meta-analysis of 9 genome-wide association studies of plasma FVII levels (7 FVII activity and 2 FVII antigen) among 27 495 participants of European and African ancestry. Each study performed ancestry-specific association analyses. Inverse variance weighted meta-analysis was performed within each ancestry group and then combined for a -ancestry meta-analysis. Our primary analysis included the 7 studies that measured FVII activity, and a secondary analysis included all 9 studies. We provided functional genomic validation for newly identified significant loci by silencing candidate genes in a human liver cell line (HuH7) using small-interfering RNA and then measuring messenger RNA and FVII protein expression. Lastly, we used meta-analysis results to perform Mendelian randomization analysis to estimate the causal effect of FVII activity on coronary artery disease, ischemic stroke (IS), and venous thromboembolism. We identified 2 novel ( and ) and 6 known loci associated with FVII activity, explaining 19.0\\% of the phenotypic variance. Adding FVII antigen data to the meta-analysis did not result in the discovery of further loci. Silencing in HuH7 cells upregulated FVII, whereas silencing downregulated FVII. Mendelian randomization analyses suggest that FVII activity has a positive causal effect on the risk of IS. Variants at and contribute to FVII activity by regulating expression levels. FVII activity appears to contribute to the etiology of IS in the general population.{\\textless}/p{\\textgreater}},\n\tjournal = {Blood},\n\tauthor = {de Vries, Paul S and Sabater-Lleal, Maria and Huffman, Jennifer E and Marten, Jonathan and Song, Ci and Pankratz, Nathan and Bartz, Traci M and de Haan, Hugoline G and Delgado, Graciela E and Eicher, John D and Martinez-Perez, Angel and Ward-Caviness, Cavin K and Brody, Jennifer A and Chen, Ming-Huei and de Maat, Moniek P M and Frånberg, Mattias and Gill, Dipender and Kleber, Marcus E and Rivadeneira, Fernando and Soria, José Manuel and Tang, Weihong and Tofler, Geoffrey H and Uitterlinden, André G and van Hylckama Vlieg, Astrid and Seshadri, Sudha and Boerwinkle, Eric and Davies, Neil M and Giese, Anne-Katrin and Ikram, M Kamran and Kittner, Steven J and McKnight, Barbara and Psaty, Bruce M and Reiner, Alex P and Sargurupremraj, Muralidharan and Taylor, Kent D and Fornage, Myriam and Hamsten, Anders and März, Winfried and Rosendaal, Frits R and Souto, Juan Carlos and Dehghan, Abbas and Johnson, Andrew D and Morrison, Alanna C and O’Donnell, Christopher J and Smith, Nicholas L},\n\tmonth = feb,\n\tyear = {2019},\n\tpages = {967--977},\n}\n\n\n\n

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\n \n\n \n \n Sáez, M E; González-Pérez, A; Hernández-Olasagarre, B; Beà, A; Moreno-Grau, S; de Rojas, I; Monté-Rubio, G; Orellana, A; Valero, S; Comella, J X; Sanchís, D; and Ruiz, A\n\n\n \n \n \n \n Genome Wide Meta-Analysis identifies common genetic signatures shared by heart function and Alzheimer’s disease.\n \n \n \n\n\n \n\n\n\n Sci Rep, 9: 16665. November 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{saez_genome_2019,\n\ttitle = {Genome {Wide} {Meta}-{Analysis} identifies common genetic signatures shared by heart function and {Alzheimer}’s disease.},\n\tvolume = {9},\n\tissn = {2045-2322},\n\tdoi = {10.1038/s41598-019-52724-2},\n\tabstract = {{\\textless}p{\\textgreater}Echocardiography has become an indispensable tool for the study of heart performance, improving the monitoring of individuals with cardiac diseases. Diverse genetic factors associated with echocardiographic measures have been previously reported. The impact of several apoptotic genes in heart development identified in experimental models prompted us to assess their potential association with human cardiac function. This study aimed at investigating the possible association of variants of apoptotic genes with echocardiographic traits and to identify new genetic markers associated with cardiac function. Genome wide data from different studies were obtained from public repositories. After quality control and imputation, a meta-analysis of individual association study results was performed. Our results confirmed the role of caspases and other apoptosis related genes with cardiac phenotypes. Moreover, enrichment analysis showed an over-representation of genes, including some apoptotic regulators, associated with Alzheimer’s disease. We further explored this unexpected observation which was confirmed by genetic correlation analyses. Our findings show the association of apoptotic gene variants with echocardiographic indicators of heart function and reveal a novel potential genetic link between echocardiographic measures in healthy populations and cognitive decline later on in life. These findings may have important implications for preventative strategies combating Alzheimer’s disease.{\\textless}/p{\\textgreater}},\n\tjournal = {Sci Rep},\n\tauthor = {Sáez, M E and González-Pérez, A and Hernández-Olasagarre, B and Beà, A and Moreno-Grau, S and de Rojas, I and Monté-Rubio, G and Orellana, A and Valero, S and Comella, J X and Sanchís, D and Ruiz, A},\n\tmonth = nov,\n\tyear = {2019},\n\tpages = {16665},\n}\n\n\n\n

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\n \n\n \n \n Kunkle, B. W; Grenier-Boley, B.; Sims, R.; Bis, J. C; Damotte, V.; Naj, A. C; Boland, A.; Vronskaya, M.; van der Lee, S. J; Amlie-Wolf, A.; Bellenguez, C.; Frizatti, A.; Chouraki, V.; Martin, E. R; Sleegers, K.; Badarinarayan, N.; Jakobsdottir, J.; Hamilton-Nelson, K. L; Moreno-Grau, S.; Olaso, R.; Raybould, R.; Chen, Y.; Kuzma, A. B; Hiltunen, M.; Morgan, T.; Ahmad, S.; Vardarajan, B. N; Epelbaum, J.; Hoffmann, P.; Boada, M.; Beecham, G. W; Garnier, J.; Harold, D.; Fitzpatrick, A. L; Valladares, O.; Moutet, M.; Gerrish, A.; Smith, A. V; Qu, L.; Bacq, D.; Denning, N.; Jian, X.; Zhao, Y.; Del Zompo, M.; Fox, N. C; Choi, S.; Mateo, I.; Hughes, J. T; Adams, H. H; Malamon, J.; Sanchez-Garcia, F.; Patel, Y.; Brody, J. A; Dombroski, B. A; Naranjo, M. C. D.; Daniilidou, M.; Eiriksdottir, G.; Mukherjee, S.; Wallon, D.; Uphill, J.; Aspelund, T.; Cantwell, L. B; Garzia, F.; Galimberti, D.; Hofer, E.; Butkiewicz, M.; Fin, B.; Scarpini, E.; Sarnowski, C.; Bush, W. S; Meslage, S.; Kornhuber, J.; White, C. C; Song, Y.; Barber, R. C; Engelborghs, S.; Sordon, S.; Voijnovic, D.; Adams, P. M; Vandenberghe, R.; Mayhaus, M.; Cupples, L A.; Albert, M. S; De Deyn, P. P; Gu, W.; Himali, J. J; Beekly, D.; Squassina, A.; Hartmann, A. M; Orellana, A.; Blacker, D.; Rodriguez-Rodriguez, E.; Lovestone, S.; Garcia, M. E; Doody, R. S; Munoz-Fernadez, C.; Sussams, R.; Lin, H.; Fairchild, T. J; Benito, Y. A; Holmes, C.; Karamujić-Čomić, H.; Frosch, M. P; Thonberg, H.; Maier, W.; Roschupkin, G.; Ghetti, B.; Giedraitis, V.; Kawalia, A.; Li, S.; Huebinger, R. M; Kilander, L.; Moebus, S.; Hernandez, I.; Kamboh, M I.; Brundin, R.; Turton, J.; Yang, Q.; Katz, M. J; Concari, L.; Lord, J.; Beiser, A. S; Keene, C D.; Helisalmi, S.; Kloszewska, I.; Kukull, W. A; Koivisto, A. M.; Lynch, A.; Tarraga, L.; Larson, E. B; Haapasalo, A.; Lawlor, B.; Mosley, T. H; Lipton, R. B; Solfrizzi, V.; Gill, M.; Longstreth, W T; Montine, T. J; Frisardi, V.; Diez-Fairen, M.; Rivadeneira, F.; Petersen, R. C; Deramecourt, V.; Alvarez, I.; Salani, F.; Ciaramella, A.; Boerwinkle, E.; Reiman, E. M; Fiévet, N.; Rotter, J. I; Reisch, J. S; Hanon, O.; Cupidi, C.; Andre Uitterlinden, A G; Royall, D. R; Dufouil, C.; Maletta, R. G.; de Rojas, I.; Sano, M.; Brice, A.; Cecchetti, R.; George-Hyslop, P. S.; Ritchie, K.; Tsolaki, M.; Tsuang, D. W; Dubois, B.; Craig, D.; Wu, C.; Soininen, H.; Avramidou, D.; Albin, R. L; Fratiglioni, L.; Germanou, A.; Apostolova, L. G; Keller, L.; Koutroumani, M.; Arnold, S. E; Panza, F.; Gkatzima, O.; Asthana, S.; Hannequin, D.; Whitehead, P.; Atwood, C. S; Caffarra, P.; Hampel, H.; Quintela, I.; Carracedo, A.; Lannfelt, L.; Rubinsztein, D. C; Barnes, L. L; Pasquier, F.; Frölich, L.; Barral, S.; McGuinness, B.; Beach, T. G; Johnston, J. A; Becker, J. T; Passmore, P.; Bigio, E. H; Schott, J. M; Bird, T. D; Warren, J. D; Boeve, B. F; Lupton, M. K; Bowen, J. D; Proitsi, P.; Boxer, A.; Powell, J. F; Burke, J. R; Kauwe, J. S K; Burns, J. M; Mancuso, M.; Buxbaum, J. D; Bonuccelli, U.; Cairns, N. J; McQuillin, A.; Cao, C.; Livingston, G.; Carlson, C. S; Bass, N. J; Carlsson, C. M; Hardy, J.; Carney, R. M; Bras, J.; Carrasquillo, M. M; Guerreiro, R.; Allen, M.; Chui, H. C; Fisher, E.; Masullo, C.; Crocco, E. A; DeCarli, C.; Bisceglio, G.; Dick, M.; Ma, L.; Duara, R.; Graff-Radford, N. R; Evans, D. A; Hodges, A.; Faber, K. M; Scherer, M.; Fallon, K. B; Riemenschneider, M.; Fardo, D. W; Heun, R.; Farlow, M. R; Kölsch, H.; Ferris, S.; Leber, M.; Foroud, T. M; Heuser, I.; Galasko, D. R; Giegling, I.; Gearing, M.; Hüll, M.; Geschwind, D. H; Gilbert, J. R; Morris, J.; Green, R. C; Mayo, K.; Growdon, J. H; Feulner, T.; Hamilton, R. L; Harrell, L. E; Drichel, D.; Honig, L. S; Cushion, T. D; Huentelman, M. J; Hollingworth, P.; Hulette, C. M; Hyman, B. T; Marshall, R.; Jarvik, G. P; Meggy, A.; Abner, E.; Menzies, G. E; Jin, L.; Leonenko, G.; Real, L. M; Jun, G. R; Baldwin, C. T; Grozeva, D.; Karydas, A.; Russo, G.; Kaye, J. A; Kim, R.; Jessen, F.; Kowall, N. W; Vellas, B.; Kramer, J. H; Vardy, E.; LaFerla, F. M; Jöckel, K.; Lah, J. J; Dichgans, M.; Leverenz, J. B; Mann, D.; Levey, A. I; Pickering-Brown, S.; Lieberman, A. P; Klopp, N.; Lunetta, K. L; Wichmann, H.; Lyketsos, C. G; Morgan, K.; Marson, D. C; Brown, K.; Martiniuk, F.; Medway, C.; Mash, D. C; Nöthen, M. M; Masliah, E.; Hooper, N. M; McCormick, W. C; Daniele, A.; McCurry, S. M; Bayer, A.; McDavid, A. N; Gallacher, J.; McKee, A. C; van den Bussche, H.; Mesulam, M.; Brayne, C.; Miller, B. L; Riedel-Heller, S.; Miller, C. A; Miller, J. W; Al-Chalabi, A.; Morris, J. C; Shaw, C. E; Myers, A. J; Wiltfang, J.; O’Bryant, S.; Olichney, J. M; Alvarez, V.; Parisi, J. E; Singleton, A. B; Paulson, H. L; Collinge, J.; Perry, W. R; Mead, S.; Peskind, E.; Cribbs, D. H; Rossor, M.; Pierce, A.; Ryan, N. S; Poon, W. W; Nacmias, B.; Potter, H.; Sorbi, S.; Quinn, J. F; Sacchinelli, E.; Raj, A.; Spalletta, G.; Raskind, M.; Caltagirone, C.; Bossù, P.; Orfei, M. D.; Reisberg, B.; Clarke, R.; Reitz, C.; Smith, A D.; Ringman, J. M; Warden, D.; Roberson, E. D; Wilcock, G.; Rogaeva, E.; Bruni, A. C.; Rosen, H. J; Gallo, M.; Rosenberg, R. N; Ben-Shlomo, Y.; Sager, M. A; Mecocci, P.; Saykin, A. J; Pastor, P.; Cuccaro, M. L; Vance, J. M; Schneider, J. A; Schneider, L. S; Slifer, S.; Seeley, W. W; Smith, A. G; Sonnen, J. A; Spina, S.; Stern, R. A; Swerdlow, R. H; Tang, M.; Tanzi, R. E; Trojanowski, J. Q; Troncoso, J. C; Van Deerlin, V. M; Van Eldik, L. J; Vinters, H. V; Vonsattel, J. P.; Weintraub, S.; Welsh-Bohmer, K. A; Wilhelmsen, K. C; Williamson, J.; Wingo, T. S; Woltjer, R. L; Wright, C. B; Yu, C.; Yu, L.; Saba, Y.; Pilotto, A.; Bullido, M. J; Peters, O.; Crane, P. K; Bennett, D.; Bosco, P.; Coto, E.; Boccardi, V.; De Jager, P. L; Lleo, A.; Warner, N.; Lopez, O. L; Ingelsson, M.; Deloukas, P.; Cruchaga, C.; Graff, C.; Gwilliam, R.; Fornage, M.; Goate, A. M; Sánchez-Juan, P.; Kehoe, P. G; Amin, N.; Ertekin-Taner, N.; Berr, C.; Debette, S.; Love, S.; Launer, L. J; Younkin, S. G; Dartigues, J.; Corcoran, C.; Ikram, M A.; Dickson, D. W; Nicolas, G.; Campion, D.; Tschanz, J.; Schmidt, H.; Hakonarson, H.; Clarimon, J.; Munger, R.; Schmidt, R.; Farrer, L. A; Van Broeckhoven, C.; C O’Donovan, M.; DeStefano, A. L; Jones, L.; Haines, J. L; Deleuze, J.; Owen, M. J; Gudnason, V.; Mayeux, R.; Escott-Price, V.; Psaty, B. M; Ramirez, A.; Wang, L.; Ruiz, A.; van Duijn, C. M; Holmans, P. A; Seshadri, S.; Williams, J.; Amouyel, P.; Schellenberg, G. D; Lambert, J.; and Pericak-Vance, M. A\n\n\n \n \n \n \n Genetic meta-analysis of diagnosed Alzheimer’s disease identifies new risk loci and implicates Aβ, tau, immunity and lipid processing.\n \n \n \n\n\n \n\n\n\n Nat Genet, 51: 414–430. March 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{kunkle_genetic_2019,\n\ttitle = {Genetic meta-analysis of diagnosed {Alzheimer}’s disease identifies new risk loci and implicates {Aβ}, tau, immunity and lipid processing.},\n\tvolume = {51},\n\tissn = {1546-1718},\n\tdoi = {10.1038/s41588-019-0358-2},\n\tabstract = {{\\textless}p{\\textgreater}Risk for late-onset Alzheimer’s disease (LOAD), the most prevalent dementia, is partially driven by genetics. To identify LOAD risk loci, we performed a large genome-wide association meta-analysis of clinically diagnosed LOAD (94,437 individuals). We confirm 20 previous LOAD risk loci and identify five new genome-wide loci (IQCK, ACE, ADAM10, ADAMTS1, and WWOX), two of which (ADAM10, ACE) were identified in a recent genome-wide association (GWAS)-by-familial-proxy of Alzheimer’s or dementia. Fine-mapping of the human leukocyte antigen (HLA) region confirms the neurological and immune-mediated disease haplotype HLA-DR15 as a risk factor for LOAD. Pathway analysis implicates immunity, lipid metabolism, tau binding proteins, and amyloid precursor protein (APP) metabolism, showing that genetic variants affecting APP and Aβ processing are associated not only with early-onset autosomal dominant Alzheimer’s disease but also with LOAD. Analyses of risk genes and pathways show enrichment for rare variants (P = 1.32 × 10), indicating that additional rare variants remain to be identified. We also identify important genetic correlations between LOAD and traits such as family history of dementia and education.{\\textless}/p{\\textgreater}},\n\tjournal = {Nat Genet},\n\tauthor = {Kunkle, Brian W and Grenier-Boley, Benjamin and Sims, Rebecca and Bis, Joshua C and Damotte, Vincent and Naj, Adam C and Boland, Anne and Vronskaya, Maria and van der Lee, Sven J and Amlie-Wolf, Alexandre and Bellenguez, Céline and Frizatti, Aura and Chouraki, Vincent and Martin, Eden R and Sleegers, Kristel and Badarinarayan, Nandini and Jakobsdottir, Johanna and Hamilton-Nelson, Kara L and Moreno-Grau, Sonia and Olaso, Robert and Raybould, Rachel and Chen, Yuning and Kuzma, Amanda B and Hiltunen, Mikko and Morgan, Taniesha and Ahmad, Shahzad and Vardarajan, Badri N and Epelbaum, Jacques and Hoffmann, Per and Boada, Merce and Beecham, Gary W and Garnier, Jean-Guillaume and Harold, Denise and Fitzpatrick, Annette L and Valladares, Otto and Moutet, Marie-Laure and Gerrish, Amy and Smith, Albert V and Qu, Liming and Bacq, Delphine and Denning, Nicola and Jian, Xueqiu and Zhao, Yi and Del Zompo, Maria and Fox, Nick C and Choi, Seung-Hoan and Mateo, Ignacio and Hughes, Joseph T and Adams, Hieab H and Malamon, John and Sanchez-Garcia, Florentino and Patel, Yogen and Brody, Jennifer A and Dombroski, Beth A and Naranjo, Maria Candida Deniz and Daniilidou, Makrina and Eiriksdottir, Gudny and Mukherjee, Shubhabrata and Wallon, David and Uphill, James and Aspelund, Thor and Cantwell, Laura B and Garzia, Fabienne and Galimberti, Daniela and Hofer, Edith and Butkiewicz, Mariusz and Fin, Bertrand and Scarpini, Elio and Sarnowski, Chloe and Bush, Will S and Meslage, Stéphane and Kornhuber, Johannes and White, Charles C and Song, Yuenjoo and Barber, Robert C and Engelborghs, Sebastiaan and Sordon, Sabrina and Voijnovic, Dina and Adams, Perrie M and Vandenberghe, Rik and Mayhaus, Manuel and Cupples, L Adrienne and Albert, Marilyn S and De Deyn, Peter P and Gu, Wei and Himali, Jayanadra J and Beekly, Duane and Squassina, Alessio and Hartmann, Annette M and Orellana, Adelina and Blacker, Deborah and Rodriguez-Rodriguez, Eloy and Lovestone, Simon and Garcia, Melissa E and Doody, Rachelle S and Munoz-Fernadez, Carmen and Sussams, Rebecca and Lin, Honghuang and Fairchild, Thomas J and Benito, Yolanda A and Holmes, Clive and Karamujić-Čomić, Hata and Frosch, Matthew P and Thonberg, Håkan and Maier, Wolfgang and Roschupkin, Gena and Ghetti, Bernardino and Giedraitis, Vilmantas and Kawalia, Amit and Li, Shuo and Huebinger, Ryan M and Kilander, Lena and Moebus, Susanne and Hernandez, Isabel and Kamboh, M Ilyas and Brundin, RoseMarie and Turton, James and Yang, Qiong and Katz, Mindy J and Concari, Letizia and Lord, Jenny and Beiser, Alexa S and Keene, C Dirk and Helisalmi, Seppo and Kloszewska, Iwona and Kukull, Walter A and Koivisto, Anne Maria and Lynch, Aoibhinn and Tarraga, Lluis and Larson, Eric B and Haapasalo, Annakaisa and Lawlor, Brian and Mosley, Thomas H and Lipton, Richard B and Solfrizzi, Vincenzo and Gill, Michael and Longstreth, W T and Montine, Thomas J and Frisardi, Vincenza and Diez-Fairen, Monica and Rivadeneira, Fernando and Petersen, Ronald C and Deramecourt, Vincent and Alvarez, Ignacio and Salani, Francesca and Ciaramella, Antonio and Boerwinkle, Eric and Reiman, Eric M and Fiévet, Nathalie and Rotter, Jerome I and Reisch, Joan S and Hanon, Olivier and Cupidi, Chiara and Andre Uitterlinden, A G and Royall, Donald R and Dufouil, Carole and Maletta, Raffaele Giovanni and de Rojas, Itziar and Sano, Mary and Brice, Alexis and Cecchetti, Roberta and George-Hyslop, Peter St and Ritchie, Karen and Tsolaki, Magda and Tsuang, Debby W and Dubois, Bruno and Craig, David and Wu, Chuang-Kuo and Soininen, Hilkka and Avramidou, Despoina and Albin, Roger L and Fratiglioni, Laura and Germanou, Antonia and Apostolova, Liana G and Keller, Lina and Koutroumani, Maria and Arnold, Steven E and Panza, Francesco and Gkatzima, Olymbia and Asthana, Sanjay and Hannequin, Didier and Whitehead, Patrice and Atwood, Craig S and Caffarra, Paolo and Hampel, Harald and Quintela, Inés and Carracedo, Angel and Lannfelt, Lars and Rubinsztein, David C and Barnes, Lisa L and Pasquier, Florence and Frölich, Lutz and Barral, Sandra and McGuinness, Bernadette and Beach, Thomas G and Johnston, Janet A and Becker, James T and Passmore, Peter and Bigio, Eileen H and Schott, Jonathan M and Bird, Thomas D and Warren, Jason D and Boeve, Bradley F and Lupton, Michelle K and Bowen, James D and Proitsi, Petra and Boxer, Adam and Powell, John F and Burke, James R and Kauwe, John S K and Burns, Jeffrey M and Mancuso, Michelangelo and Buxbaum, Joseph D and Bonuccelli, Ubaldo and Cairns, Nigel J and McQuillin, Andrew and Cao, Chuanhai and Livingston, Gill and Carlson, Chris S and Bass, Nicholas J and Carlsson, Cynthia M and Hardy, John and Carney, Regina M and Bras, Jose and Carrasquillo, Minerva M and Guerreiro, Rita and Allen, Mariet and Chui, Helena C and Fisher, Elizabeth and Masullo, Carlo and Crocco, Elizabeth A and DeCarli, Charles and Bisceglio, Gina and Dick, Malcolm and Ma, Li and Duara, Ranjan and Graff-Radford, Neill R and Evans, Denis A and Hodges, Angela and Faber, Kelley M and Scherer, Martin and Fallon, Kenneth B and Riemenschneider, Matthias and Fardo, David W and Heun, Reinhard and Farlow, Martin R and Kölsch, Heike and Ferris, Steven and Leber, Markus and Foroud, Tatiana M and Heuser, Isabella and Galasko, Douglas R and Giegling, Ina and Gearing, Marla and Hüll, Michael and Geschwind, Daniel H and Gilbert, John R and Morris, John and Green, Robert C and Mayo, Kevin and Growdon, John H and Feulner, Thomas and Hamilton, Ronald L and Harrell, Lindy E and Drichel, Dmitriy and Honig, Lawrence S and Cushion, Thomas D and Huentelman, Matthew J and Hollingworth, Paul and Hulette, Christine M and Hyman, Bradley T and Marshall, Rachel and Jarvik, Gail P and Meggy, Alun and Abner, Erin and Menzies, Georgina E and Jin, Lee-Way and Leonenko, Ganna and Real, Luis M and Jun, Gyungah R and Baldwin, Clinton T and Grozeva, Detelina and Karydas, Anna and Russo, Giancarlo and Kaye, Jeffrey A and Kim, Ronald and Jessen, Frank and Kowall, Neil W and Vellas, Bruno and Kramer, Joel H and Vardy, Emma and LaFerla, Frank M and Jöckel, Karl-Heinz and Lah, James J and Dichgans, Martin and Leverenz, James B and Mann, David and Levey, Allan I and Pickering-Brown, Stuart and Lieberman, Andrew P and Klopp, Norman and Lunetta, Kathryn L and Wichmann, H-Erich and Lyketsos, Constantine G and Morgan, Kevin and Marson, Daniel C and Brown, Kristelle and Martiniuk, Frank and Medway, Christopher and Mash, Deborah C and Nöthen, Markus M and Masliah, Eliezer and Hooper, Nigel M and McCormick, Wayne C and Daniele, Antonio and McCurry, Susan M and Bayer, Anthony and McDavid, Andrew N and Gallacher, John and McKee, Ann C and van den Bussche, Hendrik and Mesulam, Marsel and Brayne, Carol and Miller, Bruce L and Riedel-Heller, Steffi and Miller, Carol A and Miller, Joshua W and Al-Chalabi, Ammar and Morris, John C and Shaw, Christopher E and Myers, Amanda J and Wiltfang, Jens and O’Bryant, Sid and Olichney, John M and Alvarez, Victoria and Parisi, Joseph E and Singleton, Andrew B and Paulson, Henry L and Collinge, John and Perry, William R and Mead, Simon and Peskind, Elaine and Cribbs, David H and Rossor, Martin and Pierce, Aimee and Ryan, Natalie S and Poon, Wayne W and Nacmias, Benedetta and Potter, Huntington and Sorbi, Sandro and Quinn, Joseph F and Sacchinelli, Eleonora and Raj, Ashok and Spalletta, Gianfranco and Raskind, Murray and Caltagirone, Carlo and Bossù, Paola and Orfei, Maria Donata and Reisberg, Barry and Clarke, Robert and Reitz, Christiane and Smith, A David and Ringman, John M and Warden, Donald and Roberson, Erik D and Wilcock, Gordon and Rogaeva, Ekaterina and Bruni, Amalia Cecilia and Rosen, Howard J and Gallo, Maura and Rosenberg, Roger N and Ben-Shlomo, Yoav and Sager, Mark A and Mecocci, Patrizia and Saykin, Andrew J and Pastor, Pau and Cuccaro, Michael L and Vance, Jeffery M and Schneider, Julie A and Schneider, Lori S and Slifer, Susan and Seeley, William W and Smith, Amanda G and Sonnen, Joshua A and Spina, Salvatore and Stern, Robert A and Swerdlow, Russell H and Tang, Mitchell and Tanzi, Rudolph E and Trojanowski, John Q and Troncoso, Juan C and Van Deerlin, Vivianna M and Van Eldik, Linda J and Vinters, Harry V and Vonsattel, Jean Paul and Weintraub, Sandra and Welsh-Bohmer, Kathleen A and Wilhelmsen, Kirk C and Williamson, Jennifer and Wingo, Thomas S and Woltjer, Randall L and Wright, Clinton B and Yu, Chang-En and Yu, Lei and Saba, Yasaman and Pilotto, Alberto and Bullido, María J and Peters, Oliver and Crane, Paul K and Bennett, David and Bosco, Paola and Coto, Eliecer and Boccardi, Virginia and De Jager, Phil L and Lleo, Alberto and Warner, Nick and Lopez, Oscar L and Ingelsson, Martin and Deloukas, Panagiotis and Cruchaga, Carlos and Graff, Caroline and Gwilliam, Rhian and Fornage, Myriam and Goate, Alison M and Sánchez-Juan, Pascual and Kehoe, Patrick G and Amin, Najaf and Ertekin-Taner, Nilifur and Berr, Claudine and Debette, Stephanie and Love, Seth and Launer, Lenore J and Younkin, Steven G and Dartigues, Jean-François and Corcoran, Chris and Ikram, M Arfan and Dickson, Dennis W and Nicolas, Gaël and Campion, Dominique and Tschanz, JoAnn and Schmidt, Helena and Hakonarson, Hakon and Clarimon, Jordi and Munger, Ron and Schmidt, Reinhold and Farrer, Lindsay A and Van Broeckhoven, Christine and C O’Donovan, Michael and DeStefano, Anita L and Jones, Lesley and Haines, Jonathan L and Deleuze, Jean-Francois and Owen, Michael J and Gudnason, Vilmundur and Mayeux, Richard and Escott-Price, Valentina and Psaty, Bruce M and Ramirez, Alfredo and Wang, Li-San and Ruiz, Agustin and van Duijn, Cornelia M and Holmans, Peter A and Seshadri, Sudha and Williams, Julie and Amouyel, Phillippe and Schellenberg, Gerard D and Lambert, Jean-Charles and Pericak-Vance, Margaret A},\n\tmonth = mar,\n\tyear = {2019},\n\tpages = {414--430},\n}\n\n\n\n

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\n \n\n \n \n Satizabal, C. L; Adams, H. H H; Hibar, D. P; White, C. C; Knol, M. J; Stein, J. L; Scholz, M.; Sargurupremraj, M.; Jahanshad, N.; Roshchupkin, G. V; Smith, A. V; Bis, J. C; Jian, X.; Luciano, M.; Hofer, E.; Teumer, A.; van der Lee, S. J; Yang, J.; Yanek, L. R; Lee, T. V; Li, S.; Hu, Y.; Koh, J. Y.; Eicher, J. D; Desrivières, S.; Arias-Vasquez, A.; Chauhan, G.; Athanasiu, L.; Rentería, M. E; Kim, S.; Hoehn, D.; Armstrong, N. J; Chen, Q.; Holmes, A. J; den Braber, A.; Kloszewska, I.; Andersson, M.; Espeseth, T.; Grimm, O.; Abramovic, L.; Alhusaini, S.; Milaneschi, Y.; Papmeyer, M.; Axelsson, T.; Ehrlich, S.; Roiz-Santiañez, R.; Kraemer, B.; Håberg, A. K; Jones, H. J; Pike, G B.; Stein, D. J; Stevens, A.; Bralten, J.; Vernooij, M. W; Harris, T. B; Filippi, I.; Witte, A V.; Guadalupe, T.; Wittfeld, K.; Mosley, T. H; Becker, J. T; Doan, N. T.; Hagenaars, S. P; Saba, Y.; Cuellar-Partida, G.; Amin, N.; Hilal, S.; Nho, K.; Mirza-Schreiber, N.; Arfanakis, K.; Becker, D. M; Ames, D.; Goldman, A. L; Lee, P. H; Boomsma, D. I; Lovestone, S.; Giddaluru, S.; Le Hellard, S.; Mattheisen, M.; Bohlken, M. M; Kasperaviciute, D.; Schmaal, L.; Lawrie, S. M; Agartz, I.; Walton, E.; Tordesillas-Gutierrez, D.; Davies, G. E; Shin, J.; Ipser, J. C; Vinke, L. N; Hoogman, M.; Jia, T.; Burkhardt, R.; Klein, M.; Crivello, F.; Janowitz, D.; Carmichael, O.; Haukvik, U. K; Aribisala, B. S; Schmidt, H.; Strike, L. T; Cheng, C.; Risacher, S. L; Pütz, B.; Fleischman, D. A; Assareh, A. A; Mattay, V. S; Buckner, R. L; Mecocci, P.; Dale, A. M; Cichon, S.; Boks, M. P; Matarin, M.; Penninx, B. W J H; Calhoun, V. D; Chakravarty, M M.; Marquand, A. F; Macare, C.; Kharabian Masouleh, S.; Oosterlaan, J.; Amouyel, P.; Hegenscheid, K.; Rotter, J. I; Schork, A. J; Liewald, D. C M; de Zubicaray, G. I; Wong, T. Y.; Shen, L.; Sämann, P. G; Brodaty, H.; Roffman, J. L; de Geus, E. J C; Tsolaki, M.; Erk, S.; van Eijk, K. R; Cavalleri, G. L; van der Wee, N. J A; McIntosh, A. M; Gollub, R. L; Bulayeva, K. B; Bernard, M.; Richards, J. S; Himali, J. J; Loeffler, M.; Rommelse, N.; Hoffmann, W.; Westlye, L. T; Valdés Hernández, M. C; Hansell, N. K; van Erp, T. G M; Wolf, C.; Kwok, J. B J; Vellas, B.; Heinz, A.; Olde Loohuis, L. M; Delanty, N.; Ho, B.; Ching, C. R K; Shumskaya, E.; Singh, B.; Hofman, A.; van der Meer, D.; Homuth, G.; Psaty, B. M; Bastin, M. E; Montgomery, G. W; Foroud, T. M; Reppermund, S.; Hottenga, J.; Simmons, A.; Meyer-Lindenberg, A.; Cahn, W.; Whelan, C. D; van Donkelaar, M. M J; Yang, Q.; Hosten, N.; Green, R. C; Thalamuthu, A.; Mohnke, S.; Hulshoff Pol, H. E; Lin, H.; Jack, C. R; Schofield, P. R; Mühleisen, T. W; Maillard, P.; Potkin, S. G; Wen, W.; Fletcher, E.; Toga, A. W; Gruber, O.; Huentelman, M.; Davey Smith, G.; Launer, L. J; Nyberg, L.; Jönsson, E. G; Crespo-Facorro, B.; Koen, N.; Greve, D. N; Uitterlinden, A. G; Weinberger, D. R; Steen, V. M; Fedko, I. O; Groenewold, N. A; Niessen, W. J; Toro, R.; Tzourio, C.; Longstreth, W. T; Ikram, M K.; Smoller, J. W; van Tol, M.; Sussmann, J. E; Paus, T.; Lemaître, H.; Schroeter, M. L; Mazoyer, B.; Andreassen, O. A; Holsboer, F.; Depondt, C.; Veltman, D. J; Turner, J. A; Pausova, Z.; Schumann, G.; van Rooij, D.; Djurovic, S.; Deary, I. J; McMahon, K. L; Müller-Myhsok, B.; Brouwer, R. M; Soininen, H.; Pandolfo, M.; Wassink, T. H; Cheung, J. W; Wolfers, T.; Martinot, J.; Zwiers, M. P; Nauck, M.; Melle, I.; Martin, N. G; Kanai, R.; Westman, E.; Kahn, R. S; Sisodiya, S. M; White, T.; Saremi, A.; van Bokhoven, H.; Brunner, H. G; Völzke, H.; Wright, M. J; van ’t Ent, D.; Nöthen, M. M; Ophoff, R. A; Buitelaar, J. K; Fernández, G.; Sachdev, P. S; Rietschel, M.; van Haren, N. E M; Fisher, S. E; Beiser, A. S; Francks, C.; Saykin, A. J; Mather, K. A; Romanczuk-Seiferth, N.; Hartman, C. A; DeStefano, A. L; Heslenfeld, D. J; Weiner, M. W; Walter, H.; Hoekstra, P. J; Nyquist, P. A; Franke, B.; Bennett, D. A; Grabe, H. J; Johnson, A. D; Chen, C.; van Duijn, C. M; Lopez, O. L; Fornage, M.; Wardlaw, J. M; Schmidt, R.; DeCarli, C.; De Jager, P. L; Villringer, A.; Debette, S.; Gudnason, V.; Medland, S. E; Shulman, J. M; Thompson, P. M; Seshadri, S.; and Ikram, M A.\n\n\n \n \n \n \n Genetic architecture of subcortical brain structures in 38,851 individuals.\n \n \n \n\n\n \n\n\n\n Nat Genet, 51: 1624–1636. November 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{satizabal_genetic_2019,\n\ttitle = {Genetic architecture of subcortical brain structures in 38,851 individuals.},\n\tvolume = {51},\n\tissn = {1546-1718},\n\tdoi = {10.1038/s41588-019-0511-y},\n\tabstract = {{\\textless}p{\\textgreater}Subcortical brain structures are integral to motion, consciousness, emotions and learning. We identified common genetic variation related to the volumes of the nucleus accumbens, amygdala, brainstem, caudate nucleus, globus pallidus, putamen and thalamus, using genome-wide association analyses in almost 40,000 individuals from CHARGE, ENIGMA and UK Biobank. We show that variability in subcortical volumes is heritable, and identify 48 significantly associated loci (40 novel at the time of analysis). Annotation of these loci by utilizing gene expression, methylation and neuropathological data identified 199 genes putatively implicated in neurodevelopment, synaptic signaling, axonal transport, apoptosis, inflammation/infection and susceptibility to neurological disorders. This set of genes is significantly enriched for Drosophila orthologs associated with neurodevelopmental phenotypes, suggesting evolutionarily conserved mechanisms. Our findings uncover novel biology and potential drug targets underlying brain development and disease.{\\textless}/p{\\textgreater}},\n\tjournal = {Nat Genet},\n\tauthor = {Satizabal, Claudia L and Adams, Hieab H H and Hibar, Derrek P and White, Charles C and Knol, Maria J and Stein, Jason L and Scholz, Markus and Sargurupremraj, Muralidharan and Jahanshad, Neda and Roshchupkin, Gennady V and Smith, Albert V and Bis, Joshua C and Jian, Xueqiu and Luciano, Michelle and Hofer, Edith and Teumer, Alexander and van der Lee, Sven J and Yang, Jingyun and Yanek, Lisa R and Lee, Tom V and Li, Shuo and Hu, Yanhui and Koh, Jia Yu and Eicher, John D and Desrivières, Sylvane and Arias-Vasquez, Alejandro and Chauhan, Ganesh and Athanasiu, Lavinia and Rentería, Miguel E and Kim, Sungeun and Hoehn, David and Armstrong, Nicola J and Chen, Qiang and Holmes, Avram J and den Braber, Anouk and Kloszewska, Iwona and Andersson, Micael and Espeseth, Thomas and Grimm, Oliver and Abramovic, Lucija and Alhusaini, Saud and Milaneschi, Yuri and Papmeyer, Martina and Axelsson, Tomas and Ehrlich, Stefan and Roiz-Santiañez, Roberto and Kraemer, Bernd and Håberg, Asta K and Jones, Hannah J and Pike, G Bruce and Stein, Dan J and Stevens, Allison and Bralten, Janita and Vernooij, Meike W and Harris, Tamara B and Filippi, Irina and Witte, A Veronica and Guadalupe, Tulio and Wittfeld, Katharina and Mosley, Thomas H and Becker, James T and Doan, Nhat Trung and Hagenaars, Saskia P and Saba, Yasaman and Cuellar-Partida, Gabriel and Amin, Najaf and Hilal, Saima and Nho, Kwangsik and Mirza-Schreiber, Nazanin and Arfanakis, Konstantinos and Becker, Diane M and Ames, David and Goldman, Aaron L and Lee, Phil H and Boomsma, Dorret I and Lovestone, Simon and Giddaluru, Sudheer and Le Hellard, Stephanie and Mattheisen, Manuel and Bohlken, Marc M and Kasperaviciute, Dalia and Schmaal, Lianne and Lawrie, Stephen M and Agartz, Ingrid and Walton, Esther and Tordesillas-Gutierrez, Diana and Davies, Gareth E and Shin, Jean and Ipser, Jonathan C and Vinke, Louis N and Hoogman, Martine and Jia, Tianye and Burkhardt, Ralph and Klein, Marieke and Crivello, Fabrice and Janowitz, Deborah and Carmichael, Owen and Haukvik, Unn K and Aribisala, Benjamin S and Schmidt, Helena and Strike, Lachlan T and Cheng, Ching-Yu and Risacher, Shannon L and Pütz, Benno and Fleischman, Debra A and Assareh, Amelia A and Mattay, Venkata S and Buckner, Randy L and Mecocci, Patrizia and Dale, Anders M and Cichon, Sven and Boks, Marco P and Matarin, Mar and Penninx, Brenda W J H and Calhoun, Vince D and Chakravarty, M Mallar and Marquand, Andre F and Macare, Christine and Kharabian Masouleh, Shahrzad and Oosterlaan, Jaap and Amouyel, Philippe and Hegenscheid, Katrin and Rotter, Jerome I and Schork, Andrew J and Liewald, David C M and de Zubicaray, Greig I and Wong, Tien Yin and Shen, Li and Sämann, Philipp G and Brodaty, Henry and Roffman, Joshua L and de Geus, Eco J C and Tsolaki, Magda and Erk, Susanne and van Eijk, Kristel R and Cavalleri, Gianpiero L and van der Wee, Nic J A and McIntosh, Andrew M and Gollub, Randy L and Bulayeva, Kazima B and Bernard, Manon and Richards, Jennifer S and Himali, Jayandra J and Loeffler, Markus and Rommelse, Nanda and Hoffmann, Wolfgang and Westlye, Lars T and Valdés Hernández, Maria C and Hansell, Narelle K and van Erp, Theo G M and Wolf, Christiane and Kwok, John B J and Vellas, Bruno and Heinz, Andreas and Olde Loohuis, Loes M and Delanty, Norman and Ho, Beng-Choon and Ching, Christopher R K and Shumskaya, Elena and Singh, Baljeet and Hofman, Albert and van der Meer, Dennis and Homuth, Georg and Psaty, Bruce M and Bastin, Mark E and Montgomery, Grant W and Foroud, Tatiana M and Reppermund, Simone and Hottenga, Jouke-Jan and Simmons, Andrew and Meyer-Lindenberg, Andreas and Cahn, Wiepke and Whelan, Christopher D and van Donkelaar, Marjolein M J and Yang, Qiong and Hosten, Norbert and Green, Robert C and Thalamuthu, Anbupalam and Mohnke, Sebastian and Hulshoff Pol, Hilleke E and Lin, Honghuang and Jack, Clifford R and Schofield, Peter R and Mühleisen, Thomas W and Maillard, Pauline and Potkin, Steven G and Wen, Wei and Fletcher, Evan and Toga, Arthur W and Gruber, Oliver and Huentelman, Matthew and Davey Smith, George and Launer, Lenore J and Nyberg, Lars and Jönsson, Erik G and Crespo-Facorro, Benedicto and Koen, Nastassja and Greve, Douglas N and Uitterlinden, André G and Weinberger, Daniel R and Steen, Vidar M and Fedko, Iryna O and Groenewold, Nynke A and Niessen, Wiro J and Toro, Roberto and Tzourio, Christophe and Longstreth, William T and Ikram, M Kamran and Smoller, Jordan W and van Tol, Marie-Jose and Sussmann, Jessika E and Paus, Tomáš and Lemaître, Hervé and Schroeter, Matthias L and Mazoyer, Bernard and Andreassen, Ole A and Holsboer, Florian and Depondt, Chantal and Veltman, Dick J and Turner, Jessica A and Pausova, Zdenka and Schumann, Gunter and van Rooij, Daan and Djurovic, Srdjan and Deary, Ian J and McMahon, Katie L and Müller-Myhsok, Bertram and Brouwer, Rachel M and Soininen, Hilkka and Pandolfo, Massimo and Wassink, Thomas H and Cheung, Joshua W and Wolfers, Thomas and Martinot, Jean-Luc and Zwiers, Marcel P and Nauck, Matthias and Melle, Ingrid and Martin, Nicholas G and Kanai, Ryota and Westman, Eric and Kahn, René S and Sisodiya, Sanjay M and White, Tonya and Saremi, Arvin and van Bokhoven, Hans and Brunner, Han G and Völzke, Henry and Wright, Margaret J and van ’t Ent, Dennis and Nöthen, Markus M and Ophoff, Roel A and Buitelaar, Jan K and Fernández, Guillén and Sachdev, Perminder S and Rietschel, Marcella and van Haren, Neeltje E M and Fisher, Simon E and Beiser, Alexa S and Francks, Clyde and Saykin, Andrew J and Mather, Karen A and Romanczuk-Seiferth, Nina and Hartman, Catharina A and DeStefano, Anita L and Heslenfeld, Dirk J and Weiner, Michael W and Walter, Henrik and Hoekstra, Pieter J and Nyquist, Paul A and Franke, Barbara and Bennett, David A and Grabe, Hans J and Johnson, Andrew D and Chen, Christopher and van Duijn, Cornelia M and Lopez, Oscar L and Fornage, Myriam and Wardlaw, Joanna M and Schmidt, Reinhold and DeCarli, Charles and De Jager, Philip L and Villringer, Arno and Debette, Stephanie and Gudnason, Vilmundur and Medland, Sarah E and Shulman, Joshua M and Thompson, Paul M and Seshadri, Sudha and Ikram, M Arfan},\n\tmonth = nov,\n\tyear = {2019},\n\tpages = {1624--1636},\n}\n\n\n\n

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\n \n\n \n \n Karasik, D.; Zillikens, M C.; Hsu, Y.; Aghdassi, A.; Åkesson, K.; Amin, N.; Barroso, I.; Bennett, D. A; Bertram, L.; Bochud, M.; Borecki, I. B; Broer, L.; Buchman, A. S; Byberg, L.; Campbell, H.; Campos-Obando, N.; Cauley, J. A; Cawthon, P. M; Chambers, J. C; Chen, Z.; Cho, N. H; Choi, H. J.; Chou, W.; Cummings, S. R; de Groot, L. C P G M; De Jager, P. L; Demuth, I.; Diatchenko, L.; Econs, M. J; Eiriksdottir, G.; Enneman, A. W; Eriksson, J.; Eriksson, J. G; Estrada, K.; Evans, D. S; Feitosa, M. F; Fu, M.; Gieger, C.; Grallert, H.; Gudnason, V.; Lenore, L. J; Hayward, C.; Hofman, A.; Homuth, G.; Huffman, K. M; Husted, L. B; Illig, T.; Ingelsson, E.; Ittermann, T.; Jansson, J.; Johnson, T.; Biffar, R.; Jordan, J. M; Jula, A.; Karlsson, M.; Khaw, K.; Kilpeläinen, T. O; Klopp, N.; Kloth, J. S L; Koller, D. L; Kooner, J. S; Kraus, W. E; Kritchevsky, S.; Kutalik, Z.; Kuulasmaa, T.; Kuusisto, J.; Laakso, M.; Lahti, J.; Lang, T.; Langdahl, B. L; Lerch, M. M; Lewis, J. R; Lill, C.; Lind, L.; Lindgren, C.; Liu, Y.; Livshits, G.; Ljunggren, O.; Loos, R. J F; Lorentzon, M.; Luan, J.; Luben, R. N; Malkin, I.; McGuigan, F. E; Medina-Gómez, C.; Meitinger, T.; Melhus, H.; Mellström, D.; Michaëlsson, K.; Mitchell, B. D; Morris, A. P; Mosekilde, L.; Nethander, M.; Newman, A. B; O’Connell, J. R; Oostra, B. A; Orwoll, E. S; Palotie, A.; Peacock, M.; Perola, M.; Peters, A.; Prince, R. L; Psaty, B. M; Räikkönen, K.; Ralston, S. H; Ripatti, S.; Rivadeneira, F.; Robbins, J. A; Rotter, J. I; Rudan, I.; Salomaa, V.; Satterfield, S.; Schipf, S.; Shin, C. S.; Smith, A. V; Smith, S. B; Soranzo, N.; Spector, T. D; Stančáková, A.; Stefansson, K.; Steinhagen-Thiessen, E.; Stolk, L.; Streeten, E. A; Styrkarsdottir, U.; Swart, K. M A; Thompson, P.; Thomson, C. A; Thorleifsson, G.; Thorsteinsdottir, U.; Tikkanen, E.; Tranah, G. J; Uitterlinden, A. G; van Duijn, C. M; van Schoor, N. M; Vandenput, L.; Vollenweider, P.; Völzke, H.; Wactawski-Wende, J.; Walker, M.; J Wareham, N.; Waterworth, D.; Weedon, M. N; Wichmann, H.; Widen, E.; Williams, F. M K; Wilson, J. F; Wright, N. C; Yerges-Armstrong, L. M; Yu, L.; Zhang, W.; Zhao, J. H.; Zhou, Y.; Nielson, C. M; Harris, T. B; Demissie, S.; Kiel, D. P; and Ohlsson, C.\n\n\n \n \n \n \n Disentangling the genetics of lean mass.\n \n \n \n\n\n \n\n\n\n Am J Clin Nutr, 109: 276–287. February 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{karasik_disentangling_2019,\n\ttitle = {Disentangling the genetics of lean mass.},\n\tvolume = {109},\n\tissn = {1938-3207},\n\tdoi = {10.1093/ajcn/nqy272},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{Background: }Lean body mass (LM) plays an important role in mobility and metabolic function. We previously identified five loci associated with LM adjusted for fat mass in kilograms. Such an adjustment may reduce the power to identify genetic signals having an association with both lean mass and fat mass.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{Objectives: }To determine the impact of different fat mass adjustments on genetic architecture of LM and identify additional LM loci.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{Methods: }We performed genome-wide association analyses for whole-body LM (20 cohorts of European ancestry with n = 38,292) measured using dual-energy X-ray absorptiometry) or bioelectrical impedance analysis, adjusted for sex, age, age2, and height with or without fat mass adjustments (Model 1 no fat adjustment; Model 2 adjustment for fat mass as a percentage of body mass; Model 3 adjustment for fat mass in kilograms).{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{Results: }Seven single-nucleotide polymorphisms (SNPs) in separate loci, including one novel LM locus (TNRC6B), were successfully replicated in an additional 47,227 individuals from 29 cohorts. Based on the strengths of the associations in Model 1 vs Model 3, we divided the LM loci into those with an effect on both lean mass and fat mass in the same direction and refer to those as "sumo wrestler" loci (FTO and MC4R). In contrast, loci with an impact specifically on LM were termed "body builder" loci (VCAN and ADAMTSL3). Using existing available genome-wide association study databases, LM increasing alleles of SNPs in sumo wrestler loci were associated with an adverse metabolic profile, whereas LM increasing alleles of SNPs in "body builder" loci were associated with metabolic protection.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{Conclusions: }In conclusion, we identified one novel LM locus (TNRC6B). Our results suggest that a genetically determined increase in lean mass might exert either harmful or protective effects on metabolic traits, depending on its relation to fat mass.{\\textless}/p{\\textgreater}},\n\tjournal = {Am J Clin Nutr},\n\tauthor = {Karasik, David and Zillikens, M Carola and Hsu, Yi-Hsiang and Aghdassi, Ali and Åkesson, Kristina and Amin, Najaf and Barroso, Inês and Bennett, David A and Bertram, Lars and Bochud, Murielle and Borecki, Ingrid B and Broer, Linda and Buchman, Aron S and Byberg, Liisa and Campbell, Harry and Campos-Obando, Natalia and Cauley, Jane A and Cawthon, Peggy M and Chambers, John C and Chen, Zhao and Cho, Nam H and Choi, Hyung Jin and Chou, Wen-Chi and Cummings, Steven R and de Groot, Lisette C P G M and De Jager, Phillip L and Demuth, Ilja and Diatchenko, Luda and Econs, Michael J and Eiriksdottir, Gudny and Enneman, Anke W and Eriksson, Joel and Eriksson, Johan G and Estrada, Karol and Evans, Daniel S and Feitosa, Mary F and Fu, Mao and Gieger, Christian and Grallert, Harald and Gudnason, Vilmundur and Lenore, Launer J and Hayward, Caroline and Hofman, Albert and Homuth, Georg and Huffman, Kim M and Husted, Lise B and Illig, Thomas and Ingelsson, Erik and Ittermann, Till and Jansson, John-Olov and Johnson, Toby and Biffar, Reiner and Jordan, Joanne M and Jula, Antti and Karlsson, Magnus and Khaw, Kay-Tee and Kilpeläinen, Tuomas O and Klopp, Norman and Kloth, Jacqueline S L and Koller, Daniel L and Kooner, Jaspal S and Kraus, William E and Kritchevsky, Stephen and Kutalik, Zoltán and Kuulasmaa, Teemu and Kuusisto, Johanna and Laakso, Markku and Lahti, Jari and Lang, Thomas and Langdahl, Bente L and Lerch, Markus M and Lewis, Joshua R and Lill, Christina and Lind, Lars and Lindgren, Cecilia and Liu, Yongmei and Livshits, Gregory and Ljunggren, Osten and Loos, Ruth J F and Lorentzon, Mattias and Luan, Jian’an and Luben, Robert N and Malkin, Ida and McGuigan, Fiona E and Medina-Gómez, Carolina and Meitinger, Thomas and Melhus, Håkan and Mellström, Dan and Michaëlsson, Karl and Mitchell, Braxton D and Morris, Andrew P and Mosekilde, Leif and Nethander, Maria and Newman, Anne B and O’Connell, Jeffery R and Oostra, Ben A and Orwoll, Eric S and Palotie, Aarno and Peacock, Munro and Perola, Markus and Peters, Annette and Prince, Richard L and Psaty, Bruce M and Räikkönen, Katri and Ralston, Stuart H and Ripatti, Samuli and Rivadeneira, Fernando and Robbins, John A and Rotter, Jerome I and Rudan, Igor and Salomaa, Veikko and Satterfield, Suzanne and Schipf, Sabine and Shin, Chan Soo and Smith, Albert V and Smith, Shad B and Soranzo, Nicole and Spector, Timothy D and Stančáková, Alena and Stefansson, Kari and Steinhagen-Thiessen, Elisabeth and Stolk, Lisette and Streeten, Elizabeth A and Styrkarsdottir, Unnur and Swart, Karin M A and Thompson, Patricia and Thomson, Cynthia A and Thorleifsson, Gudmar and Thorsteinsdottir, Unnur and Tikkanen, Emmi and Tranah, Gregory J and Uitterlinden, André G and van Duijn, Cornelia M and van Schoor, Natasja M and Vandenput, Liesbeth and Vollenweider, Peter and Völzke, Henry and Wactawski-Wende, Jean and Walker, Mark and J Wareham, Nicholas and Waterworth, Dawn and Weedon, Michael N and Wichmann, H-Erich and Widen, Elisabeth and Williams, Frances M K and Wilson, James F and Wright, Nicole C and Yerges-Armstrong, Laura M and Yu, Lei and Zhang, Weihua and Zhao, Jing Hua and Zhou, Yanhua and Nielson, Carrie M and Harris, Tamara B and Demissie, Serkalem and Kiel, Douglas P and Ohlsson, Claes},\n\tmonth = feb,\n\tyear = {2019},\n\tpages = {276--287},\n}\n\n\n\n

\n\n\n

\n \\textlessp\\textgreater\\textbfBackground: Lean body mass (LM) plays an important role in mobility and metabolic function. We previously identified five loci associated with LM adjusted for fat mass in kilograms. Such an adjustment may reduce the power to identify genetic signals having an association with both lean mass and fat mass.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfObjectives: To determine the impact of different fat mass adjustments on genetic architecture of LM and identify additional LM loci.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfMethods: We performed genome-wide association analyses for whole-body LM (20 cohorts of European ancestry with n = 38,292) measured using dual-energy X-ray absorptiometry) or bioelectrical impedance analysis, adjusted for sex, age, age2, and height with or without fat mass adjustments (Model 1 no fat adjustment; Model 2 adjustment for fat mass as a percentage of body mass; Model 3 adjustment for fat mass in kilograms).\\textless/p\\textgreater\\textlessp\\textgreater\\textbfResults: Seven single-nucleotide polymorphisms (SNPs) in separate loci, including one novel LM locus (TNRC6B), were successfully replicated in an additional 47,227 individuals from 29 cohorts. Based on the strengths of the associations in Model 1 vs Model 3, we divided the LM loci into those with an effect on both lean mass and fat mass in the same direction and refer to those as \"sumo wrestler\" loci (FTO and MC4R). In contrast, loci with an impact specifically on LM were termed \"body builder\" loci (VCAN and ADAMTSL3). Using existing available genome-wide association study databases, LM increasing alleles of SNPs in sumo wrestler loci were associated with an adverse metabolic profile, whereas LM increasing alleles of SNPs in \"body builder\" loci were associated with metabolic protection.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfConclusions: In conclusion, we identified one novel LM locus (TNRC6B). Our results suggest that a genetically determined increase in lean mass might exert either harmful or protective effects on metabolic traits, depending on its relation to fat mass.\\textless/p\\textgreater\n

\n\n\n

\n \n\n \n \n Barfield, R.; Wang, H.; Liu, Y.; Brody, J. A; Swenson, B.; Li, R.; Bartz, T. M; Sotoodehnia, N.; Chen, Y. I; Cade, B. E; Chen, H.; Patel, S. R; Zhu, X.; Gharib, S. A; Johnson, W C.; Rotter, J. I; Saxena, R.; Purcell, S.; Lin, X.; Redline, S.; and Sofer, T.\n\n\n \n \n \n \n Epigenome-wide association analysis of daytime sleepiness in the Multi-Ethnic Study of Atherosclerosis reveals African-American-specific associations.\n \n \n \n\n\n \n\n\n\n Sleep. May 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{barfield_epigenome-wide_2019,\n\ttitle = {Epigenome-wide association analysis of daytime sleepiness in the {Multi}-{Ethnic} {Study} of {Atherosclerosis} reveals {African}-{American}-specific associations.},\n\tissn = {1550-9109},\n\tdoi = {10.1093/sleep/zsz101},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{STUDY OBJECTIVES: }Daytime sleepiness is a consequence of inadequate sleep, sleep-wake control disorder, or other medical conditions. Population variability in prevalence of daytime sleepiness is likely due to genetic and biological factors as well as social and environmental influences. DNA methylation (DNAm) potentially influences multiple health outcomes. Here, we explored the association between DNAm and daytime sleepiness quantified by the Epworth Sleepiness Scale (ESS).{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS: }We performed multi-ethnic and ethnic-specific epigenome-wide association studies for DNAm and ESS in the Multi-Ethnic Study of Atherosclerosis (MESA; n = 619) and the Cardiovascular Health Study (n = 483), with cross-study replication and meta-analysis. Genetic variants near ESS-associated DNAm were analyzed for methylation quantitative trait loci and followed with replication of genotype-sleepiness associations in the UK Biobank.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{RESULTS: }In MESA only, we detected four DNAm-ESS associations: one across all race/ethnic groups; three in African-Americans (AA) only. Two of the MESA AA associations, in genes KCTD5 and RXRA, nominally replicated in CHS (p-value {\\textless} 0.05). In the AA meta-analysis, we detected 14 DNAm-ESS associations (FDR q-value {\\textless} 0.05, top association p-value = 4.26 × 10-8). Three DNAm sites mapped to genes (CPLX3, GFAP, and C7orf50) with biological relevance. We also found evidence for associations with DNAm sites in RAI1, a gene associated with sleep and circadian phenotypes. UK Biobank follow-up analyses detected SNPs in RAI1, RXRA, and CPLX3 with nominal sleepiness associations.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSIONS: }We identified methylation sites in multiple genes possibly implicated in daytime sleepiness. Most significant DNAm-ESS associations were specific to AA. Future work is needed to identify mechanisms driving ancestry-specific methylation effects.{\\textless}/p{\\textgreater}},\n\tjournal = {Sleep},\n\tauthor = {Barfield, Richard and Wang, Heming and Liu, Yongmei and Brody, Jennifer A and Swenson, Brenton and Li, Ruitong and Bartz, Traci M and Sotoodehnia, Nona and Chen, Yii-der I and Cade, Brian E and Chen, Han and Patel, Sanjay R and Zhu, Xiaofeng and Gharib, Sina A and Johnson, W Craig and Rotter, Jerome I and Saxena, Richa and Purcell, Shaun and Lin, Xihong and Redline, Susan and Sofer, Tamar},\n\tmonth = may,\n\tyear = {2019},\n}\n\n\n\n

\n\n\n

\n \\textlessp\\textgreater\\textbfSTUDY OBJECTIVES: Daytime sleepiness is a consequence of inadequate sleep, sleep-wake control disorder, or other medical conditions. Population variability in prevalence of daytime sleepiness is likely due to genetic and biological factors as well as social and environmental influences. DNA methylation (DNAm) potentially influences multiple health outcomes. Here, we explored the association between DNAm and daytime sleepiness quantified by the Epworth Sleepiness Scale (ESS).\\textless/p\\textgreater\\textlessp\\textgreater\\textbfMETHODS: We performed multi-ethnic and ethnic-specific epigenome-wide association studies for DNAm and ESS in the Multi-Ethnic Study of Atherosclerosis (MESA; n = 619) and the Cardiovascular Health Study (n = 483), with cross-study replication and meta-analysis. Genetic variants near ESS-associated DNAm were analyzed for methylation quantitative trait loci and followed with replication of genotype-sleepiness associations in the UK Biobank.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfRESULTS: In MESA only, we detected four DNAm-ESS associations: one across all race/ethnic groups; three in African-Americans (AA) only. Two of the MESA AA associations, in genes KCTD5 and RXRA, nominally replicated in CHS (p-value \\textless 0.05). In the AA meta-analysis, we detected 14 DNAm-ESS associations (FDR q-value \\textless 0.05, top association p-value = 4.26 × 10-8). Three DNAm sites mapped to genes (CPLX3, GFAP, and C7orf50) with biological relevance. We also found evidence for associations with DNAm sites in RAI1, a gene associated with sleep and circadian phenotypes. UK Biobank follow-up analyses detected SNPs in RAI1, RXRA, and CPLX3 with nominal sleepiness associations.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfCONCLUSIONS: We identified methylation sites in multiple genes possibly implicated in daytime sleepiness. Most significant DNAm-ESS associations were specific to AA. Future work is needed to identify mechanisms driving ancestry-specific methylation effects.\\textless/p\\textgreater\n

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\n \n\n \n \n Bhatt, S. P; Balte, P. P; Schwartz, J. E; Cassano, P. A; Couper, D.; Jacobs, D. R; Kalhan, R.; O’Connor, G. T; Yende, S.; Sanders, J. L; Umans, J. G; Dransfield, M. T; Chaves, P. H; White, W. B; and Oelsner, E. C\n\n\n \n \n \n \n Discriminative Accuracy of FEV1:FVC Thresholds for COPD-Related Hospitalization and Mortality.\n \n \n \n\n\n \n\n\n\n JAMA, 321: 2438–2447. 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{bhatt_discriminative_2019,\n\ttitle = {Discriminative {Accuracy} of {FEV1}:{FVC} {Thresholds} for {COPD}-{Related} {Hospitalization} and {Mortality}.},\n\tvolume = {321},\n\tissn = {1538-3598},\n\tdoi = {10.1001/jama.2019.7233},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{Importance: }According to numerous current guidelines, the diagnosis of chronic obstructive pulmonary disease (COPD) requires a ratio of the forced expiratory volume in the first second to the forced vital capacity (FEV1:FVC) of less than 0.70, yet this fixed threshold is based on expert opinion and remains controversial.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{Objective: }To determine the discriminative accuracy of various FEV1:FVC fixed thresholds for predicting COPD-related hospitalization and mortality.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{Design, Setting, and Participants: }The National Heart, Lung, and Blood Institute (NHLBI) Pooled Cohorts Study harmonized and pooled data from 4 US general population-based cohorts (Atherosclerosis Risk in Communities Study; Cardiovascular Health Study; Health, Aging, and Body Composition Study; and Multi-Ethnic Study of Atherosclerosis). Participants aged 45 to 102 years were enrolled from 1987 to 2000 and received follow-up longitudinally through 2016.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{Exposures: }Presence of airflow obstruction, which was defined by a baseline FEV1:FVC less than a range of fixed thresholds (0.75 to 0.65) or less than the lower limit of normal as defined by Global Lung Initiative reference equations (LLN).{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{Main Outcomes and Measures: }The primary outcome was a composite of COPD hospitalization and COPD-related mortality, defined by adjudication or administrative criteria. The optimal fixed FEV1:FVC threshold was defined by the best discrimination for these COPD-related events as indexed using the Harrell C statistic from unadjusted Cox proportional hazards models. Differences in C statistics were compared with respect to less than 0.70 and less than LLN thresholds using a nonparametric approach.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{Results: }Among 24 207 adults in the pooled cohort (mean [SD] age at enrollment, 63 [10.5] years; 12 990 [54\\%] women; 16 794 [69\\%] non-Hispanic white; 15 181 [63\\%] ever smokers), complete follow-up was available for 11 077 (77\\%) at 15 years. During a median follow-up of 15 years, 3925 participants experienced COPD-related events over 340 757 person-years of follow-up (incidence density rate, 11.5 per 1000 person-years), including 3563 COPD-related hospitalizations and 447 COPD-related deaths. With respect to discrimination of COPD-related events, the optimal fixed threshold (0.71; C statistic for optimal fixed threshold, 0.696) was not significantly different from the 0.70 threshold (difference, 0.001 [95\\% CI, -0.002 to 0.004]) but was more accurate than the LLN threshold (difference, 0.034 [95\\% CI, 0.028 to 0.041]). The 0.70 threshold provided optimal discrimination in the subgroup analysis of ever smokers and in adjusted models.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{Conclusions and Relevance: }Defining airflow obstruction as FEV1:FVC less than 0.70 provided discrimination of COPD-related hospitalization and mortality that was not significantly different or was more accurate than other fixed thresholds and the LLN. These results support the use of FEV1:FVC less than 0.70 to identify individuals at risk of clinically significant COPD.{\\textless}/p{\\textgreater}},\n\tjournal = {JAMA},\n\tauthor = {Bhatt, Surya P and Balte, Pallavi P and Schwartz, Joseph E and Cassano, Patricia A and Couper, David and Jacobs, David R and Kalhan, Ravi and O’Connor, George T and Yende, Sachin and Sanders, Jason L and Umans, Jason G and Dransfield, Mark T and Chaves, Paulo H and White, Wendy B and Oelsner, Elizabeth C},\n\tyear = {2019},\n\tkeywords = {80 and over, Aged, Chronic Obstructive, Cohort Studies, Female, Forced Expiratory Volume, Hospitalization, Humans, Male, Middle Aged, Prognosis, Proportional Hazards Models, Pulmonary Disease, Risk Assessment, Vital Capacity},\n\tpages = {2438--2447},\n}\n\n\n\n

\n\n\n

\n \\textlessp\\textgreater\\textbfImportance: According to numerous current guidelines, the diagnosis of chronic obstructive pulmonary disease (COPD) requires a ratio of the forced expiratory volume in the first second to the forced vital capacity (FEV1:FVC) of less than 0.70, yet this fixed threshold is based on expert opinion and remains controversial.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfObjective: To determine the discriminative accuracy of various FEV1:FVC fixed thresholds for predicting COPD-related hospitalization and mortality.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfDesign, Setting, and Participants: The National Heart, Lung, and Blood Institute (NHLBI) Pooled Cohorts Study harmonized and pooled data from 4 US general population-based cohorts (Atherosclerosis Risk in Communities Study; Cardiovascular Health Study; Health, Aging, and Body Composition Study; and Multi-Ethnic Study of Atherosclerosis). Participants aged 45 to 102 years were enrolled from 1987 to 2000 and received follow-up longitudinally through 2016.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfExposures: Presence of airflow obstruction, which was defined by a baseline FEV1:FVC less than a range of fixed thresholds (0.75 to 0.65) or less than the lower limit of normal as defined by Global Lung Initiative reference equations (LLN).\\textless/p\\textgreater\\textlessp\\textgreater\\textbfMain Outcomes and Measures: The primary outcome was a composite of COPD hospitalization and COPD-related mortality, defined by adjudication or administrative criteria. The optimal fixed FEV1:FVC threshold was defined by the best discrimination for these COPD-related events as indexed using the Harrell C statistic from unadjusted Cox proportional hazards models. Differences in C statistics were compared with respect to less than 0.70 and less than LLN thresholds using a nonparametric approach.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfResults: Among 24 207 adults in the pooled cohort (mean [SD] age at enrollment, 63 [10.5] years; 12 990 [54%] women; 16 794 [69%] non-Hispanic white; 15 181 [63%] ever smokers), complete follow-up was available for 11 077 (77%) at 15 years. During a median follow-up of 15 years, 3925 participants experienced COPD-related events over 340 757 person-years of follow-up (incidence density rate, 11.5 per 1000 person-years), including 3563 COPD-related hospitalizations and 447 COPD-related deaths. With respect to discrimination of COPD-related events, the optimal fixed threshold (0.71; C statistic for optimal fixed threshold, 0.696) was not significantly different from the 0.70 threshold (difference, 0.001 [95% CI, -0.002 to 0.004]) but was more accurate than the LLN threshold (difference, 0.034 [95% CI, 0.028 to 0.041]). The 0.70 threshold provided optimal discrimination in the subgroup analysis of ever smokers and in adjusted models.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfConclusions and Relevance: Defining airflow obstruction as FEV1:FVC less than 0.70 provided discrimination of COPD-related hospitalization and mortality that was not significantly different or was more accurate than other fixed thresholds and the LLN. These results support the use of FEV1:FVC less than 0.70 to identify individuals at risk of clinically significant COPD.\\textless/p\\textgreater\n

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\n \n\n \n \n Xue, Q.; Tian, J.; Walston, J. D; Chaves, P. H M; Newman, A. B; and Bandeen-Roche, K.\n\n\n \n \n \n \n Discrepancy in Frailty Identification: Move beyond Predictive Validity.\n \n \n \n\n\n \n\n\n\n J Gerontol A Biol Sci Med Sci. February 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{xue_discrepancy_2019,\n\ttitle = {Discrepancy in {Frailty} {Identification}: {Move} beyond {Predictive} {Validity}.},\n\tissn = {1758-535X},\n\tdoi = {10.1093/gerona/glz052},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{BACKGROUND: }To evaluate the discordance in frailty classification between the frailty index (FI) and the physical frailty phenotype (PFP) and identify factors discriminating those with discordant frailty classification from each other and from those for whom the assessments agree.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS: }A prospective observational study of older adults aged 65 and older selected from Medicare eligibility lists in four US communities (n=5,362). The PFP was measured by the Cardiovascular Health Study PFP. Subjects meeting {\\textgreater}=3 of the 5 criteria were deemed frail. The FI was calculated as the proportion of deficits in an a priori selected set of 48 measures and subjects were classified as frail if FI{\\textgreater}0.35.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{RESULTS: }The prevalence of frailty was 7.0\\% by the PFP and 8.3\\% by the FI. Of the 730 deemed frail by either instrument, only 12\\% were in agreement; whereas 39\\% were classified as frail by PFP but not FI; and 48\\% were classified as frail by FI but not PFP. Participants aged 65-72 or greater disease burden were mostly likely to be characterized as being FI-frail but not PFP-frail. The associations of frailty with age and mortality was stronger when frailty was measured by the PFP rather than the FI.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSIONS: }Despite comparable frailty prevalence between the PFP and the FI, there was substantial discordance in individual-level classification, with highest agreement existing only in the most vulnerable subset. These findings suggest that there are clinically important contexts in which PFP and FI cannot be used interchangeably.{\\textless}/p{\\textgreater}},\n\tjournal = {J Gerontol A Biol Sci Med Sci},\n\tauthor = {Xue, Qian-Li and Tian, Jing and Walston, Jeremy D and Chaves, Paulo H M and Newman, Anne B and Bandeen-Roche, Karen},\n\tmonth = feb,\n\tyear = {2019},\n}\n\n\n\n

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\n \n\n \n \n \n\n\n \n \n \n \n Dairy Intake and Body Composition and Cardiometabolic Traits among Adults: Mendelian Randomization Analysis of 182041 Individuals from 18 Studies.\n \n \n \n\n\n \n\n\n\n Clin Chem, 65: 751–760. June 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{noauthor_dairy_2019,\n\ttitle = {Dairy {Intake} and {Body} {Composition} and {Cardiometabolic} {Traits} among {Adults}: {Mendelian} {Randomization} {Analysis} of 182041 {Individuals} from 18 {Studies}.},\n\tvolume = {65},\n\tissn = {1530-8561},\n\tdoi = {10.1373/clinchem.2018.300335},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{BACKGROUND: }Associations between dairy intake and body composition and cardiometabolic traits have been inconsistently observed in epidemiological studies, and the causal relationship remains ill-defined.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS: }We performed Mendelian randomization analysis using an established genetic variant located upstream of the lactase gene (-13910 C/T, rs4988235) associated with dairy intake as an instrumental variable (IV). The causal effects of dairy intake on body composition and cardiometabolic traits (lipids, glycemic traits, and inflammatory factors) were quantified by IV estimators among 182041 participants from 18 studies.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{RESULTS: }Each 1 serving/day higher dairy intake was associated with higher lean mass [β (SE) = 0.117 kg (0.035); = 0.001], higher hemoglobin A [0.009\\% (0.002); {\\textless} 0.001], lower LDL [-0.014 mmol/L (0.006); = 0.013], total cholesterol (TC) [-0.012 mmol/L (0.005); = 0.023], and non-HDL [-0.012 mmol/L (0.005); = 0.028]. The -13910 C/T CT + TT genotype was associated with 0.214 more dairy servings/day (SE = 0.047; {\\textless} 0.001), 0.284 cm higher waist circumference (SE = 0.118; = 0.017), 0.112 kg higher lean mass (SE = 0.027; = 3.8 × 10), 0.032 mmol/L lower LDL (SE = 0.009; = 0.001), and 0.032 mmol/L lower TC (SE = 0.010; = 0.001). Genetically higher dairy intake was associated with increased lean mass [0.523 kg per serving/day (0.170); = 0.002] after correction for multiple testing (0.05/18). However, we find that genetically higher dairy intake was not associated with lipids and glycemic traits.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSIONS: }The present study provides evidence to support a potential causal effect of higher dairy intake on increased lean mass among adults. Our findings suggest that the observational associations of dairy intake with lipids and glycemic traits may be the result of confounding.{\\textless}/p{\\textgreater}},\n\tjournal = {Clin Chem},\n\tmonth = jun,\n\tyear = {2019},\n\tpages = {751--760},\n}\n\n\n\n

\n\n\n

\n \\textlessp\\textgreater\\textbfBACKGROUND: Associations between dairy intake and body composition and cardiometabolic traits have been inconsistently observed in epidemiological studies, and the causal relationship remains ill-defined.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfMETHODS: We performed Mendelian randomization analysis using an established genetic variant located upstream of the lactase gene (-13910 C/T, rs4988235) associated with dairy intake as an instrumental variable (IV). The causal effects of dairy intake on body composition and cardiometabolic traits (lipids, glycemic traits, and inflammatory factors) were quantified by IV estimators among 182041 participants from 18 studies.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfRESULTS: Each 1 serving/day higher dairy intake was associated with higher lean mass [β (SE) = 0.117 kg (0.035); = 0.001], higher hemoglobin A [0.009% (0.002); \\textless 0.001], lower LDL [-0.014 mmol/L (0.006); = 0.013], total cholesterol (TC) [-0.012 mmol/L (0.005); = 0.023], and non-HDL [-0.012 mmol/L (0.005); = 0.028]. The -13910 C/T CT + TT genotype was associated with 0.214 more dairy servings/day (SE = 0.047; \\textless 0.001), 0.284 cm higher waist circumference (SE = 0.118; = 0.017), 0.112 kg higher lean mass (SE = 0.027; = 3.8 × 10), 0.032 mmol/L lower LDL (SE = 0.009; = 0.001), and 0.032 mmol/L lower TC (SE = 0.010; = 0.001). Genetically higher dairy intake was associated with increased lean mass [0.523 kg per serving/day (0.170); = 0.002] after correction for multiple testing (0.05/18). However, we find that genetically higher dairy intake was not associated with lipids and glycemic traits.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfCONCLUSIONS: The present study provides evidence to support a potential causal effect of higher dairy intake on increased lean mass among adults. Our findings suggest that the observational associations of dairy intake with lipids and glycemic traits may be the result of confounding.\\textless/p\\textgreater\n

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\n \n\n \n \n Dörr, M.; Hamburg, N. M; Müller, C.; Smith, N. L; Gustafsson, S.; Lehtimäki, T.; Teumer, A.; Zeller, T.; Li, X.; Lind, L.; Raitakari, O. T; Völker, U.; Blankenberg, S.; McKnight, B.; Morris, A. P; Kähönen, M.; Lemaitre, R. N; Wild, P. S; Nauck, M.; Völzke, H.; Münzel, T.; Mitchell, G. F; Psaty, B. M; Lindgren, C. M; Larson, M. G; Felix, S. B; Ingelsson, E.; Lyytikäinen, L.; Herrington, D.; Benjamin, E. J; and Schnabel, R. B\n\n\n \n \n \n \n Common Genetic Variation in Relation to Brachial Vascular Dimensions and Flow-Mediated Vasodilation.\n \n \n \n\n\n \n\n\n\n Circ Genom Precis Med, 12: e002409. February 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{dorr_common_2019,\n\ttitle = {Common {Genetic} {Variation} in {Relation} to {Brachial} {Vascular} {Dimensions} and {Flow}-{Mediated} {Vasodilation}.},\n\tvolume = {12},\n\tissn = {2574-8300},\n\tdoi = {10.1161/CIRCGEN.118.002409},\n\tjournal = {Circ Genom Precis Med},\n\tauthor = {Dörr, Marcus and Hamburg, Naomi M and Müller, Christian and Smith, Nicholas L and Gustafsson, Stefan and Lehtimäki, Terho and Teumer, Alexander and Zeller, Tanja and Li, Xiaohui and Lind, Lars and Raitakari, Olli T and Völker, Uwe and Blankenberg, Stefan and McKnight, Barbara and Morris, Andrew P and Kähönen, Mika and Lemaitre, Rozenn N and Wild, Philipp S and Nauck, Matthias and Völzke, Henry and Münzel, Thomas and Mitchell, Gary F and Psaty, Bruce M and Lindgren, Cecilia M and Larson, Martin G and Felix, Stephan B and Ingelsson, Erik and Lyytikäinen, Leo-Pekka and Herrington, David and Benjamin, Emelia J and Schnabel, Renate B},\n\tmonth = feb,\n\tyear = {2019},\n\tpages = {e002409},\n}\n\n\n\n

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\n \n\n \n \n Massera, D; Xu, S; Walker, M D; Valderrábano, R J; Mukamal, K J; Ix, J H; Siscovick, D S; Tracy, R P; Robbins, J A; Biggs, M L; Xue, X; and Kizer, J R\n\n\n \n \n \n \n Biochemical markers of bone turnover and risk of incident hip fracture in older women: the Cardiovascular Health Study.\n \n \n \n\n\n \n\n\n\n Osteoporos Int. June 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{massera_biochemical_2019,\n\ttitle = {Biochemical markers of bone turnover and risk of incident hip fracture in older women: the {Cardiovascular} {Health} {Study}.},\n\tissn = {1433-2965},\n\tdoi = {10.1007/s00198-019-05043-1},\n\tabstract = {{\\textless}p{\\textgreater}The relationships of osteocalcin (OC) and C-telopeptide of type I collagen (CTX) with long-term incidence of hip fracture were examined in 1680 post-menopausal women from a population-based study. CTX, but not OC, levels were associated with incident hip fracture in these participants, a relationship characterized by an inverted U-shape.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{INTRODUCTION: }We sought to investigate the relationships of OC, a marker of bone formation, and CTX, a marker of bone resorption, with long-term incidence of hip fracture in older women.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS: }We included 1680 women from the population-based Cardiovascular Health Study (mean [SD] age 74.5 [5.0] years). The longitudinal association of both markers with incidence of hip fracture was examined using multivariable Cox models.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{RESULTS: }During a median follow-up of 12.3 years, 288 incident hip fractures occurred. Linear spline analysis did not demonstrate an association between OC levels and incident hip fracture. By contrast, increasing levels of CTX up to the middle-upper range were associated with a significantly greater risk of hip fracture (HR = 1.52 per SD increment, 95\\% CI = 1.10-2.09), while further increases were associated with a marginally non-significant lower risk (HR = 0.80 per SD increment, 95\\% CI = 0.63-1.01), after full adjustment for potential confounders. In analyses of quartiles, CTX exhibited a similar inverted U-shaped relationship with incident fracture after adjustment, with a significant association observed only for the comparison of quartile 3 to quartile 1 (HR = 1.63, 95\\% CI = 1.10-2.43). In a subset with available measures, both OC and CTX were inversely associated with bone mineral density of the hip.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSION: }CTX, but not OC, levels were associated with incident hip fracture in post-menopausal women, a relationship characterized by an inverted U-shape. These findings highlight the complex relationship of bone turnover markers with hip fracture risk.{\\textless}/p{\\textgreater}},\n\tjournal = {Osteoporos Int},\n\tauthor = {Massera, D and Xu, S and Walker, M D and Valderrábano, R J and Mukamal, K J and Ix, J H and Siscovick, D S and Tracy, R P and Robbins, J A and Biggs, M L and Xue, X and Kizer, J R},\n\tmonth = jun,\n\tyear = {2019},\n}\n\n\n\n

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\n \\textlessp\\textgreaterThe relationships of osteocalcin (OC) and C-telopeptide of type I collagen (CTX) with long-term incidence of hip fracture were examined in 1680 post-menopausal women from a population-based study. CTX, but not OC, levels were associated with incident hip fracture in these participants, a relationship characterized by an inverted U-shape.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfINTRODUCTION: We sought to investigate the relationships of OC, a marker of bone formation, and CTX, a marker of bone resorption, with long-term incidence of hip fracture in older women.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfMETHODS: We included 1680 women from the population-based Cardiovascular Health Study (mean [SD] age 74.5 [5.0] years). The longitudinal association of both markers with incidence of hip fracture was examined using multivariable Cox models.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfRESULTS: During a median follow-up of 12.3 years, 288 incident hip fractures occurred. Linear spline analysis did not demonstrate an association between OC levels and incident hip fracture. By contrast, increasing levels of CTX up to the middle-upper range were associated with a significantly greater risk of hip fracture (HR = 1.52 per SD increment, 95% CI = 1.10-2.09), while further increases were associated with a marginally non-significant lower risk (HR = 0.80 per SD increment, 95% CI = 0.63-1.01), after full adjustment for potential confounders. In analyses of quartiles, CTX exhibited a similar inverted U-shaped relationship with incident fracture after adjustment, with a significant association observed only for the comparison of quartile 3 to quartile 1 (HR = 1.63, 95% CI = 1.10-2.43). In a subset with available measures, both OC and CTX were inversely associated with bone mineral density of the hip.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfCONCLUSION: CTX, but not OC, levels were associated with incident hip fracture in post-menopausal women, a relationship characterized by an inverted U-shape. These findings highlight the complex relationship of bone turnover markers with hip fracture risk.\\textless/p\\textgreater\n

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\n \n\n \n \n Wuttke, M.; Li, Y.; Li, M.; Sieber, K. B; Feitosa, M. F; Gorski, M.; Tin, A.; Wang, L.; Chu, A. Y; Hoppmann, A.; Kirsten, H.; Giri, A.; Chai, J.; Sveinbjornsson, G.; Tayo, B. O; Nutile, T.; Fuchsberger, C.; Marten, J.; Cocca, M.; Ghasemi, S.; Xu, Y.; Horn, K.; Noce, D.; van der Most, P. J; Sedaghat, S.; Yu, Z.; Akiyama, M.; Afaq, S.; Ahluwalia, T. S; Almgren, P.; Amin, N.; Arnlöv, J.; Bakker, S. J L; Bansal, N.; Baptista, D.; Bergmann, S.; Biggs, M. L; Biino, G.; Boehnke, M.; Boerwinkle, E.; Boissel, M.; Bottinger, E. P; Boutin, T. S; Brenner, H.; Brumat, M.; Burkhardt, R.; Butterworth, A. S; Campana, E.; Campbell, A.; Campbell, H.; Canouil, M.; Carroll, R. J; Catamo, E.; Chambers, J. C; Chee, M.; Chee, M.; Chen, X.; Cheng, C.; Cheng, Y.; Christensen, K.; Cifkova, R.; Ciullo, M.; Concas, M. P.; Cook, J. P; Coresh, J.; Corre, T.; Sala, C. F.; Cusi, D.; Danesh, J.; Daw, E W.; de Borst, M. H; De Grandi, A.; de Mutsert, R.; de Vries, A. P J; Degenhardt, F.; Delgado, G.; Demirkan, A.; Di Angelantonio, E.; Dittrich, K.; Divers, J.; Dorajoo, R.; Eckardt, K.; Ehret, G.; Elliott, P.; Endlich, K.; Evans, M. K; Felix, J. F; Foo, V. H. X.; Franco, O. H; Franke, A.; Freedman, B. I; Freitag-Wolf, S.; Friedlander, Y.; Froguel, P.; Gansevoort, R. T; Gao, H.; Gasparini, P.; Gaziano, J M.; Giedraitis, V.; Gieger, C.; Girotto, G.; Giulianini, F.; Gögele, M.; Gordon, S. D; Gudbjartsson, D. F; Gudnason, V.; Haller, T.; Hamet, P.; Harris, T. B; Hartman, C. A; Hayward, C.; Hellwege, J. N; Heng, C.; Hicks, A. A; Hofer, E.; Huang, W.; Hutri-Kähönen, N.; Hwang, S.; Ikram, M A.; Indridason, O. S; Ingelsson, E.; Ising, M.; Jaddoe, V. W V; Jakobsdottir, J.; Jonas, J. B; Joshi, P. K; Josyula, N. S.; Jung, B.; Kähönen, M.; Kamatani, Y.; Kammerer, C. M; Kanai, M.; Kastarinen, M.; Kerr, S. M; Khor, C.; Kiess, W.; Kleber, M. E; Koenig, W.; Kooner, J. S; Körner, A.; Kovacs, P.; Kraja, A. T; Krajcoviechova, A.; Kramer, H.; Krämer, B. K; Kronenberg, F.; Kubo, M.; Kuhnel, B.; Kuokkanen, M.; Kuusisto, J.; La Bianca, M.; Laakso, M.; Lange, L. A; Langefeld, C. D; Lee, J. J.; Lehne, B.; Lehtimäki, T.; Lieb, W.; Lim, S.; Lind, L.; Lindgren, C. M; Liu, J.; Liu, J.; Loeffler, M.; Loos, R. J F; Lucae, S.; Lukas, M. A.; Lyytikäinen, L.; Mägi, R.; Magnusson, P. K E; Mahajan, A.; Martin, N. G; Martins, J.; März, W.; Mascalzoni, D.; Matsuda, K.; Meisinger, C.; Meitinger, T.; Melander, O.; Metspalu, A.; Mikaelsdottir, E. K; Milaneschi, Y.; Miliku, K.; Mishra, P. P; Mohlke, K. L; Mononen, N.; Montgomery, G. W; Mook-Kanamori, D. O; Mychaleckyj, J. C; Nadkarni, G. N; Nalls, M. A; Nauck, M.; Nikus, K.; Ning, B.; Nolte, I. M; Noordam, R.; O’Connell, J.; O’Donoghue, M. L; Olafsson, I.; Oldehinkel, A. J; Orho-Melander, M.; Ouwehand, W. H; Padmanabhan, S.; Palmer, N. D; Palsson, R.; Penninx, B. W J H; Perls, T.; Perola, M.; Pirastu, M.; Pirastu, N.; Pistis, G.; Podgornaia, A. I; Polasek, O.; Ponte, B.; Porteous, D. J; Poulain, T.; Pramstaller, P. P; Preuss, M. H; Prins, B. P; Province, M. A; Rabelink, T. J; Raffield, L. M; Raitakari, O. T; Reilly, D. F; Rettig, R.; Rheinberger, M.; Rice, K. M; Ridker, P. M; Rivadeneira, F.; Rizzi, F.; Roberts, D. J; Robino, A.; Rossing, P.; Rudan, I.; Rueedi, R.; Ruggiero, D.; Ryan, K. A; Saba, Y.; Sabanayagam, C.; Salomaa, V.; Salvi, E.; Saum, K.; Schmidt, H.; Schmidt, R.; Schöttker, B.; Schulz, C.; Schupf, N.; Shaffer, C. M; Shi, Y.; Smith, A. V; Smith, B. H; Soranzo, N.; Spracklen, C. N; Strauch, K.; Stringham, H. M; Stumvoll, M.; Svensson, P. O; Szymczak, S.; Tai, E.; Tajuddin, S. M; Tan, N. Y Q; Taylor, K. D; Teren, A.; Tham, Y.; Thiery, J.; Thio, C. H L; Thomsen, H.; Thorleifsson, G.; Toniolo, D.; Tönjes, A.; Tremblay, J.; Tzoulaki, I.; Uitterlinden, A. G; Vaccargiu, S.; van Dam, R. M; van der Harst, P.; van Duijn, C. M; Velez Edward, D. R; Verweij, N.; Vogelezang, S.; Völker, U.; Vollenweider, P.; Waeber, G.; Waldenberger, M.; Wallentin, L.; Wang, Y. X.; Wang, C.; Waterworth, D. M; Bin Wei, W.; White, H.; Whitfield, J. B; Wild, S. H; Wilson, J. F; Wojczynski, M. K; Wong, C.; Wong, T.; Xu, L.; Yang, Q.; Yasuda, M.; Yerges-Armstrong, L. M; Zhang, W.; Zonderman, A. B; Rotter, J. I; Bochud, M.; Psaty, B. M; Vitart, V.; Wilson, J. G; Dehghan, A.; Parsa, A.; Chasman, D. I; Ho, K.; Morris, A. P; Devuyst, O.; Akilesh, S.; Pendergrass, S. A; Sim, X.; Böger, C. A; Okada, Y.; Edwards, T. L; Snieder, H.; Stefansson, K.; Hung, A. M; Heid, I. M; Scholz, M.; Teumer, A.; Köttgen, A.; and Pattaro, C.\n\n\n \n \n \n \n A catalog of genetic loci associated with kidney function from analyses of a million individuals.\n \n \n \n\n\n \n\n\n\n Nat Genet, 51: 957–972. 2019.\n \n\n\n\n
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@article{wuttke_catalog_2019,\n\ttitle = {A catalog of genetic loci associated with kidney function from analyses of a million individuals.},\n\tvolume = {51},\n\tissn = {1546-1718},\n\tdoi = {10.1038/s41588-019-0407-x},\n\tabstract = {{\\textless}p{\\textgreater}Chronic kidney disease (CKD) is responsible for a public health burden with multi-systemic complications. Through trans-ancestry meta-analysis of genome-wide association studies of estimated glomerular filtration rate (eGFR) and independent replication (n = 1,046,070), we identified 264 associated loci (166 new). Of these, 147 were likely to be relevant for kidney function on the basis of associations with the alternative kidney function marker blood urea nitrogen (n = 416,178). Pathway and enrichment analyses, including mouse models with renal phenotypes, support the kidney as the main target organ. A genetic risk score for lower eGFR was associated with clinically diagnosed CKD in 452,264 independent individuals. Colocalization analyses of associations with eGFR among 783,978 European-ancestry individuals and gene expression across 46 human tissues, including tubulo-interstitial and glomerular kidney compartments, identified 17 genes differentially expressed in kidney. Fine-mapping highlighted missense driver variants in 11 genes and kidney-specific regulatory variants. These results provide a comprehensive priority list of molecular targets for translational research.{\\textless}/p{\\textgreater}},\n\tjournal = {Nat Genet},\n\tauthor = {Wuttke, Matthias and Li, Yong and Li, Man and Sieber, Karsten B and Feitosa, Mary F and Gorski, Mathias and Tin, Adrienne and Wang, Lihua and Chu, Audrey Y and Hoppmann, Anselm and Kirsten, Holger and Giri, Ayush and Chai, Jin-Fang and Sveinbjornsson, Gardar and Tayo, Bamidele O and Nutile, Teresa and Fuchsberger, Christian and Marten, Jonathan and Cocca, Massimiliano and Ghasemi, Sahar and Xu, Yizhe and Horn, Katrin and Noce, Damia and van der Most, Peter J and Sedaghat, Sanaz and Yu, Zhi and Akiyama, Masato and Afaq, Saima and Ahluwalia, Tarunveer S and Almgren, Peter and Amin, Najaf and Arnlöv, Johan and Bakker, Stephan J L and Bansal, Nisha and Baptista, Daniela and Bergmann, Sven and Biggs, Mary L and Biino, Ginevra and Boehnke, Michael and Boerwinkle, Eric and Boissel, Mathilde and Bottinger, Erwin P and Boutin, Thibaud S and Brenner, Hermann and Brumat, Marco and Burkhardt, Ralph and Butterworth, Adam S and Campana, Eric and Campbell, Archie and Campbell, Harry and Canouil, Mickaël and Carroll, Robert J and Catamo, Eulalia and Chambers, John C and Chee, Miao-Ling and Chee, Miao-Li and Chen, Xu and Cheng, Ching-Yu and Cheng, Yurong and Christensen, Kaare and Cifkova, Renata and Ciullo, Marina and Concas, Maria Pina and Cook, James P and Coresh, Josef and Corre, Tanguy and Sala, Cinzia Felicita and Cusi, Daniele and Danesh, John and Daw, E Warwick and de Borst, Martin H and De Grandi, Alessandro and de Mutsert, Renée and de Vries, Aiko P J and Degenhardt, Frauke and Delgado, Graciela and Demirkan, Ayse and Di Angelantonio, Emanuele and Dittrich, Katalin and Divers, Jasmin and Dorajoo, Rajkumar and Eckardt, Kai-Uwe and Ehret, Georg and Elliott, Paul and Endlich, Karlhans and Evans, Michele K and Felix, Janine F and Foo, Valencia Hui Xian and Franco, Oscar H and Franke, Andre and Freedman, Barry I and Freitag-Wolf, Sandra and Friedlander, Yechiel and Froguel, Philippe and Gansevoort, Ron T and Gao, He and Gasparini, Paolo and Gaziano, J Michael and Giedraitis, Vilmantas and Gieger, Christian and Girotto, Giorgia and Giulianini, Franco and Gögele, Martin and Gordon, Scott D and Gudbjartsson, Daniel F and Gudnason, Vilmundur and Haller, Toomas and Hamet, Pavel and Harris, Tamara B and Hartman, Catharina A and Hayward, Caroline and Hellwege, Jacklyn N and Heng, Chew-Kiat and Hicks, Andrew A and Hofer, Edith and Huang, Wei and Hutri-Kähönen, Nina and Hwang, Shih-Jen and Ikram, M Arfan and Indridason, Olafur S and Ingelsson, Erik and Ising, Marcus and Jaddoe, Vincent W V and Jakobsdottir, Johanna and Jonas, Jost B and Joshi, Peter K and Josyula, Navya Shilpa and Jung, Bettina and Kähönen, Mika and Kamatani, Yoichiro and Kammerer, Candace M and Kanai, Masahiro and Kastarinen, Mika and Kerr, Shona M and Khor, Chiea-Chuen and Kiess, Wieland and Kleber, Marcus E and Koenig, Wolfgang and Kooner, Jaspal S and Körner, Antje and Kovacs, Peter and Kraja, Aldi T and Krajcoviechova, Alena and Kramer, Holly and Krämer, Bernhard K and Kronenberg, Florian and Kubo, Michiaki and Kuhnel, Brigitte and Kuokkanen, Mikko and Kuusisto, Johanna and La Bianca, Martina and Laakso, Markku and Lange, Leslie A and Langefeld, Carl D and Lee, Jeannette Jen-Mai and Lehne, Benjamin and Lehtimäki, Terho and Lieb, Wolfgang and Lim, Su-Chi and Lind, Lars and Lindgren, Cecilia M and Liu, Jun and Liu, Jianjun and Loeffler, Markus and Loos, Ruth J F and Lucae, Susanne and Lukas, Mary Ann and Lyytikäinen, Leo-Pekka and Mägi, Reedik and Magnusson, Patrik K E and Mahajan, Anubha and Martin, Nicholas G and Martins, Jade and März, Winfried and Mascalzoni, Deborah and Matsuda, Koichi and Meisinger, Christa and Meitinger, Thomas and Melander, Olle and Metspalu, Andres and Mikaelsdottir, Evgenia K and Milaneschi, Yuri and Miliku, Kozeta and Mishra, Pashupati P and Mohlke, Karen L and Mononen, Nina and Montgomery, Grant W and Mook-Kanamori, Dennis O and Mychaleckyj, Josyf C and Nadkarni, Girish N and Nalls, Mike A and Nauck, Matthias and Nikus, Kjell and Ning, Boting and Nolte, Ilja M and Noordam, Raymond and O’Connell, Jeffrey and O’Donoghue, Michelle L and Olafsson, Isleifur and Oldehinkel, Albertine J and Orho-Melander, Marju and Ouwehand, Willem H and Padmanabhan, Sandosh and Palmer, Nicholette D and Palsson, Runolfur and Penninx, Brenda W J H and Perls, Thomas and Perola, Markus and Pirastu, Mario and Pirastu, Nicola and Pistis, Giorgio and Podgornaia, Anna I and Polasek, Ozren and Ponte, Belen and Porteous, David J and Poulain, Tanja and Pramstaller, Peter P and Preuss, Michael H and Prins, Bram P and Province, Michael A and Rabelink, Ton J and Raffield, Laura M and Raitakari, Olli T and Reilly, Dermot F and Rettig, Rainer and Rheinberger, Myriam and Rice, Kenneth M and Ridker, Paul M and Rivadeneira, Fernando and Rizzi, Federica and Roberts, David J and Robino, Antonietta and Rossing, Peter and Rudan, Igor and Rueedi, Rico and Ruggiero, Daniela and Ryan, Kathleen A and Saba, Yasaman and Sabanayagam, Charumathi and Salomaa, Veikko and Salvi, Erika and Saum, Kai-Uwe and Schmidt, Helena and Schmidt, Reinhold and Schöttker, Ben and Schulz, Christina-Alexandra and Schupf, Nicole and Shaffer, Christian M and Shi, Yuan and Smith, Albert V and Smith, Blair H and Soranzo, Nicole and Spracklen, Cassandra N and Strauch, Konstantin and Stringham, Heather M and Stumvoll, Michael and Svensson, Per O and Szymczak, Silke and Tai, E-Shyong and Tajuddin, Salman M and Tan, Nicholas Y Q and Taylor, Kent D and Teren, Andrej and Tham, Yih-Chung and Thiery, Joachim and Thio, Chris H L and Thomsen, Hauke and Thorleifsson, Gudmar and Toniolo, Daniela and Tönjes, Anke and Tremblay, Johanne and Tzoulaki, Ioanna and Uitterlinden, André G and Vaccargiu, Simona and van Dam, Rob M and van der Harst, Pim and van Duijn, Cornelia M and Velez Edward, Digna R and Verweij, Niek and Vogelezang, Suzanne and Völker, Uwe and Vollenweider, Peter and Waeber, Gérard and Waldenberger, Melanie and Wallentin, Lars and Wang, Ya Xing and Wang, Chaolong and Waterworth, Dawn M and Bin Wei, Wen and White, Harvey and Whitfield, John B and Wild, Sarah H and Wilson, James F and Wojczynski, Mary K and Wong, Charlene and Wong, Tien-Yin and Xu, Liang and Yang, Qiong and Yasuda, Masayuki and Yerges-Armstrong, Laura M and Zhang, Weihua and Zonderman, Alan B and Rotter, Jerome I and Bochud, Murielle and Psaty, Bruce M and Vitart, Veronique and Wilson, James G and Dehghan, Abbas and Parsa, Afshin and Chasman, Daniel I and Ho, Kevin and Morris, Andrew P and Devuyst, Olivier and Akilesh, Shreeram and Pendergrass, Sarah A and Sim, Xueling and Böger, Carsten A and Okada, Yukinori and Edwards, Todd L and Snieder, Harold and Stefansson, Kari and Hung, Adriana M and Heid, Iris M and Scholz, Markus and Teumer, Alexander and Köttgen, Anna and Pattaro, Cristian},\n\tyear = {2019},\n\tkeywords = {Chromosome Mapping, Chronic, European Continental Ancestry Group, Genetic Association Studies, Genetic Predisposition to Disease, Genome-Wide Association Study, Glomerular Filtration Rate, Heritable, Humans, Inheritance Patterns, Kidney Function Tests, Phenotype, Polymorphism, Quantitative Trait, Quantitative Trait Loci, Renal Insufficiency, Single Nucleotide, Uromodulin},\n\tpages = {957--972},\n}\n\n\n\n

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\n \n\n \n \n Marklund, M.; Wu, J. H Y; Imamura, F.; Del Gobbo, L. C; Fretts, A.; de Goede, J.; Shi, P.; Tintle, N.; Wennberg, M.; Aslibekyan, S.; Chen, T.; de Oliveira Otto, M. C; Hirakawa, Y.; Eriksen, H. H.; Kröger, J.; Laguzzi, F.; Lankinen, M.; Murphy, R. A; Prem, K.; Samieri, C.; Virtanen, J.; Wood, A. C; Wong, K.; Yang, W.; Zhou, X.; Baylin, A.; Boer, J. M A; Brouwer, I. A; Campos, H.; Chaves, P. H M; Chien, K.; de Faire, U.; Djoussé, L.; Eiriksdottir, G.; El-Abbadi, N.; Forouhi, N. G; Michael Gaziano, J; Geleijnse, J. M; Gigante, B.; Giles, G.; Guallar, E.; Gudnason, V.; Harris, T.; Harris, W. S; Helmer, C.; Hellenius, M.; Hodge, A.; Hu, F. B; Jacques, P. F; Jansson, J.; Kalsbeek, A.; Khaw, K.; Koh, W.; Laakso, M.; Leander, K.; Lin, H.; Lind, L.; Luben, R.; Luo, J.; McKnight, B.; Mursu, J.; Ninomiya, T.; Overvad, K.; Psaty, B. M; Rimm, E.; Schulze, M. B; Siscovick, D.; Skjelbo Nielsen, M.; Smith, A. V; Steffen, B. T; Steffen, L.; Sun, Q.; Sundström, J.; Tsai, M. Y; Tunstall-Pedoe, H.; Uusitupa, M. I J; van Dam, R. M; Veenstra, J.; Monique Verschuren, W M; Wareham, N.; Willett, W.; Woodward, M.; Yuan, J.; Micha, R.; Lemaitre, R. N; Mozaffarian, D.; and Riserus, U.\n\n\n \n \n \n \n Biomarkers of Dietary Omega-6 Fatty Acids and Incident Cardiovascular Disease and Mortality.\n \n \n \n\n\n \n\n\n\n Circulation, 139: 2422–2436. May 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{marklund_biomarkers_2019,\n\ttitle = {Biomarkers of {Dietary} {Omega}-6 {Fatty} {Acids} and {Incident} {Cardiovascular} {Disease} and {Mortality}.},\n\tvolume = {139},\n\tissn = {1524-4539},\n\tdoi = {10.1161/CIRCULATIONAHA.118.038908},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{BACKGROUND: }Global dietary recommendations for and cardiovascular effects of linoleic acid, the major dietary omega-6 fatty acid, and its major metabolite, arachidonic acid, remain controversial. To address this uncertainty and inform international recommendations, we evaluated how in vivo circulating and tissue levels of linoleic acid (LA) and arachidonic acid (AA) relate to incident cardiovascular disease (CVD) across multiple international studies.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS: }We performed harmonized, de novo, individual-level analyses in a global consortium of 30 prospective observational studies from 13 countries. Multivariable-adjusted associations of circulating and adipose tissue LA and AA biomarkers with incident total CVD and subtypes (coronary heart disease, ischemic stroke, cardiovascular mortality) were investigated according to a prespecified analytic plan. Levels of LA and AA, measured as the percentage of total fatty acids, were evaluated linearly according to their interquintile range (ie, the range between the midpoint of the first and fifth quintiles), and categorically by quintiles. Study-specific results were pooled using inverse-variance-weighted meta-analysis. Heterogeneity was explored by age, sex, race, diabetes mellitus, statin use, aspirin use, omega-3 levels, and fatty acid desaturase 1 genotype (when available).{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{RESULTS: }In 30 prospective studies with medians of follow-up ranging 2.5 to 31.9 years, 15 198 incident cardiovascular events occurred among 68 659 participants. Higher levels of LA were significantly associated with lower risks of total CVD, cardiovascular mortality, and ischemic stroke, with hazard ratios per interquintile range of 0.93 (95\\% CI, 0.88-0.99), 0.78 (0.70-0.85), and 0.88 (0.79-0.98), respectively, and nonsignificantly with lower coronary heart disease risk (0.94; 0.88-1.00). Relationships were similar for LA evaluated across quintiles. AA levels were not associated with higher risk of cardiovascular outcomes; in a comparison of extreme quintiles, higher levels were associated with lower risk of total CVD (0.92; 0.86-0.99). No consistent heterogeneity by population subgroups was identified in the observed relationships.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSIONS: }In pooled global analyses, higher in vivo circulating and tissue levels of LA and possibly AA were associated with lower risk of major cardiovascular events. These results support a favorable role for LA in CVD prevention.{\\textless}/p{\\textgreater}},\n\tjournal = {Circulation},\n\tauthor = {Marklund, Matti and Wu, Jason H Y and Imamura, Fumiaki and Del Gobbo, Liana C and Fretts, Amanda and de Goede, Janette and Shi, Peilin and Tintle, Nathan and Wennberg, Maria and Aslibekyan, Stella and Chen, Tzu-An and de Oliveira Otto, Marcia C and Hirakawa, Yoichiro and Eriksen, Helle Højmark and Kröger, Janine and Laguzzi, Federica and Lankinen, Maria and Murphy, Rachel A and Prem, Kiesha and Samieri, Cecilia and Virtanen, Jyrki and Wood, Alexis C and Wong, Kerry and Yang, Wei-Sin and Zhou, Xia and Baylin, Ana and Boer, Jolanda M A and Brouwer, Ingeborg A and Campos, Hannia and Chaves, Paulo H M and Chien, Kuo-Liong and de Faire, Ulf and Djoussé, Luc and Eiriksdottir, Gudny and El-Abbadi, Naglaa and Forouhi, Nita G and Michael Gaziano, J and Geleijnse, Johanna M and Gigante, Bruna and Giles, Graham and Guallar, Eliseo and Gudnason, Vilmundur and Harris, Tamara and Harris, William S and Helmer, Catherine and Hellenius, Mai-Lis and Hodge, Allison and Hu, Frank B and Jacques, Paul F and Jansson, Jan-Håkan and Kalsbeek, Anya and Khaw, Kay-Tee and Koh, Woon-Puay and Laakso, Markku and Leander, Karin and Lin, Hung-Ju and Lind, Lars and Luben, Robert and Luo, Juhua and McKnight, Barbara and Mursu, Jaakko and Ninomiya, Toshiharu and Overvad, Kim and Psaty, Bruce M and Rimm, Eric and Schulze, Matthias B and Siscovick, David and Skjelbo Nielsen, Michael and Smith, Albert V and Steffen, Brian T and Steffen, Lyn and Sun, Qi and Sundström, Johan and Tsai, Michael Y and Tunstall-Pedoe, Hugh and Uusitupa, Matti I J and van Dam, Rob M and Veenstra, Jenna and Monique Verschuren, W M and Wareham, Nick and Willett, Walter and Woodward, Mark and Yuan, Jian-Min and Micha, Renata and Lemaitre, Rozenn N and Mozaffarian, Dariush and Riserus, Ulf},\n\tmonth = may,\n\tyear = {2019},\n\tpages = {2422--2436},\n}\n\n\n\n

\n\n\n

\n \\textlessp\\textgreater\\textbfBACKGROUND: Global dietary recommendations for and cardiovascular effects of linoleic acid, the major dietary omega-6 fatty acid, and its major metabolite, arachidonic acid, remain controversial. To address this uncertainty and inform international recommendations, we evaluated how in vivo circulating and tissue levels of linoleic acid (LA) and arachidonic acid (AA) relate to incident cardiovascular disease (CVD) across multiple international studies.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfMETHODS: We performed harmonized, de novo, individual-level analyses in a global consortium of 30 prospective observational studies from 13 countries. Multivariable-adjusted associations of circulating and adipose tissue LA and AA biomarkers with incident total CVD and subtypes (coronary heart disease, ischemic stroke, cardiovascular mortality) were investigated according to a prespecified analytic plan. Levels of LA and AA, measured as the percentage of total fatty acids, were evaluated linearly according to their interquintile range (ie, the range between the midpoint of the first and fifth quintiles), and categorically by quintiles. Study-specific results were pooled using inverse-variance-weighted meta-analysis. Heterogeneity was explored by age, sex, race, diabetes mellitus, statin use, aspirin use, omega-3 levels, and fatty acid desaturase 1 genotype (when available).\\textless/p\\textgreater\\textlessp\\textgreater\\textbfRESULTS: In 30 prospective studies with medians of follow-up ranging 2.5 to 31.9 years, 15 198 incident cardiovascular events occurred among 68 659 participants. Higher levels of LA were significantly associated with lower risks of total CVD, cardiovascular mortality, and ischemic stroke, with hazard ratios per interquintile range of 0.93 (95% CI, 0.88-0.99), 0.78 (0.70-0.85), and 0.88 (0.79-0.98), respectively, and nonsignificantly with lower coronary heart disease risk (0.94; 0.88-1.00). Relationships were similar for LA evaluated across quintiles. AA levels were not associated with higher risk of cardiovascular outcomes; in a comparison of extreme quintiles, higher levels were associated with lower risk of total CVD (0.92; 0.86-0.99). No consistent heterogeneity by population subgroups was identified in the observed relationships.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfCONCLUSIONS: In pooled global analyses, higher in vivo circulating and tissue levels of LA and possibly AA were associated with lower risk of major cardiovascular events. These results support a favorable role for LA in CVD prevention.\\textless/p\\textgreater\n

\n\n\n

\n \n\n \n \n Cade, B. E; Chen, H.; Stilp, A. M; Louie, T.; Ancoli-Israel, S.; Arens, R.; Barfield, R.; Below, J. E; Cai, J.; Conomos, M. P; Evans, D. S; Frazier-Wood, A. C; Gharib, S. A; Gleason, K. J; Gottlieb, D. J; Hillman, D. R; Johnson, W C.; Lederer, D. J; Lee, J.; Loredo, J. S; Mei, H.; Mukherjee, S.; Patel, S. R; Post, W. S; Purcell, S. M; Ramos, A. R; Reid, K. J; Rice, K.; Shah, N. A; Sofer, T.; Taylor, K. D; Thornton, T. A; Wang, H.; Yaffe, K.; Zee, P. C; Hanis, C. L; Palmer, L. J; Rotter, J. I; Stone, K. L; Tranah, G. J; Wilson, J. G; Sunyaev, S. R; Laurie, C. C; Zhu, X.; Saxena, R.; Lin, X.; and Redline, S.\n\n\n \n \n \n \n Associations of variants In the hexokinase 1 and interleukin 18 receptor regions with oxyhemoglobin saturation during sleep.\n \n \n \n\n\n \n\n\n\n PLoS Genet, 15: e1007739. 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{cade_associations_2019,\n\ttitle = {Associations of variants {In} the hexokinase 1 and interleukin 18 receptor regions with oxyhemoglobin saturation during sleep.},\n\tvolume = {15},\n\tissn = {1553-7404},\n\tdoi = {10.1371/journal.pgen.1007739},\n\tabstract = {{\\textless}p{\\textgreater}Sleep disordered breathing (SDB)-related overnight hypoxemia is associated with cardiometabolic disease and other comorbidities. Understanding the genetic bases for variations in nocturnal hypoxemia may help understand mechanisms influencing oxygenation and SDB-related mortality. We conducted genome-wide association tests across 10 cohorts and 4 populations to identify genetic variants associated with three correlated measures of overnight oxyhemoglobin saturation: average and minimum oxyhemoglobin saturation during sleep and the percent of sleep with oxyhemoglobin saturation under 90\\%. The discovery sample consisted of 8,326 individuals. Variants with p {\\textless} 1 × 10(-6) were analyzed in a replication group of 14,410 individuals. We identified 3 significantly associated regions, including 2 regions in multi-ethnic analyses (2q12, 10q22). SNPs in the 2q12 region associated with minimum SpO2 (rs78136548 p = 2.70 × 10(-10)). SNPs at 10q22 were associated with all three traits including average SpO2 (rs72805692 p = 4.58 × 10(-8)). SNPs in both regions were associated in over 20,000 individuals and are supported by prior associations or functional evidence. Four additional significant regions were detected in secondary sex-stratified and combined discovery and replication analyses, including a region overlapping Reelin, a known marker of respiratory complex neurons.These are the first genome-wide significant findings reported for oxyhemoglobin saturation during sleep, a phenotype of high clinical interest. Our replicated associations with HK1 and IL18R1 suggest that variants in inflammatory pathways, such as the biologically-plausible NLRP3 inflammasome, may contribute to nocturnal hypoxemia.{\\textless}/p{\\textgreater}},\n\tjournal = {PLoS Genet},\n\tauthor = {Cade, Brian E and Chen, Han and Stilp, Adrienne M and Louie, Tin and Ancoli-Israel, Sonia and Arens, Raanan and Barfield, Richard and Below, Jennifer E and Cai, Jianwen and Conomos, Matthew P and Evans, Daniel S and Frazier-Wood, Alexis C and Gharib, Sina A and Gleason, Kevin J and Gottlieb, Daniel J and Hillman, David R and Johnson, W Craig and Lederer, David J and Lee, Jiwon and Loredo, Jose S and Mei, Hao and Mukherjee, Sutapa and Patel, Sanjay R and Post, Wendy S and Purcell, Shaun M and Ramos, Alberto R and Reid, Kathryn J and Rice, Ken and Shah, Neomi A and Sofer, Tamar and Taylor, Kent D and Thornton, Timothy A and Wang, Heming and Yaffe, Kristine and Zee, Phyllis C and Hanis, Craig L and Palmer, Lyle J and Rotter, Jerome I and Stone, Katie L and Tranah, Gregory J and Wilson, James G and Sunyaev, Shamil R and Laurie, Cathy C and Zhu, Xiaofeng and Saxena, Richa and Lin, Xihong and Redline, Susan},\n\tyear = {2019},\n\tkeywords = {80 and over, Adolescent, Adult, Aged, Cell Adhesion Molecules, Computational Biology, Extracellular Matrix Proteins, Female, Gene Regulatory Networks, Genetic Variation, Genome-Wide Association Study, Hexokinase, Humans, Hypoxia, Interleukin-18 Receptor alpha Subunit, Male, Middle Aged, NLR Family, Nerve Tissue Proteins, Neuronal, Oxygen, Oxyhemoglobins, Polymorphism, Pyrin Domain-Containing 3 Protein, Quantitative Trait Loci, Serine Endopeptidases, Single Nucleotide, Sleep, Sleep Apnea Syndromes, Young Adult},\n\tpages = {e1007739},\n}\n\n\n\n

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\n \n\n \n \n Clark, D. W; Okada, Y.; Moore, K. H S; Mason, D.; Pirastu, N.; Gandin, I.; Mattsson, H.; Barnes, C. L K; Lin, K.; Zhao, J. H.; Deelen, P.; Rohde, R.; Schurmann, C.; Guo, X.; Giulianini, F.; Zhang, W.; Medina-Gómez, C.; Karlsson, R.; Bao, Y.; Bartz, T. M; Baumbach, C.; Biino, G.; Bixley, M. J; Brumat, M.; Chai, J.; Corre, T.; Cousminer, D. L; Dekker, A. M; Eccles, D. A; van Eijk, K. R; Fuchsberger, C.; Gao, H.; Germain, M.; Gordon, S. D; de Haan, H. G; Harris, S. E; Hofer, E.; Huerta-Chagoya, A.; Igartua, C.; Jansen, I. E; Jia, Y.; Kacprowski, T.; Karlsson, T.; Kleber, M. E; Li, S. A.; Li-Gao, R.; Mahajan, A.; Matsuda, K.; Meidtner, K.; Meng, W.; Montasser, M. E; van der Most, P. J; Munz, M.; Nutile, T.; Palviainen, T.; Prasad, G.; Prasad, R. B; Priyanka, T. D. S.; Rizzi, F.; Salvi, E.; Sapkota, B. R; Shriner, D.; Skotte, L.; Smart, M. C; Smith, A. V.; van der Spek, A.; Spracklen, C. N; Strawbridge, R. J; Tajuddin, S. M; Trompet, S.; Turman, C.; Verweij, N.; Viberti, C.; Wang, L.; Warren, H. R; Wootton, R. E; Yanek, L. R; Yao, J.; Yousri, N. A; Zhao, W.; Adeyemo, A. A; Afaq, S.; Aguilar-Salinas, C. A.; Akiyama, M.; Albert, M. L; Allison, M. A; Alver, M.; Aung, T.; Azizi, F.; Bentley, A. R; Boeing, H.; Boerwinkle, E.; Borja, J. B; de Borst, G. J; Bottinger, E. P; Broer, L.; Campbell, H.; Chanock, S.; Chee, M.; Chen, G.; Chen, Y. I; Chen, Z.; Chiu, Y.; Cocca, M.; Collins, F. S; Concas, M. P.; Corley, J.; Cugliari, G.; van Dam, R. M; Damulina, A.; Daneshpour, M. S; Day, F. R; Delgado, G. E; Dhana, K.; Doney, A. S F; Dörr, M.; Doumatey, A. P; Dzimiri, N.; Ebenesersdóttir, S S.; Elliott, J.; Elliott, P.; Ewert, R.; Felix, J. F; Fischer, K.; Freedman, B. I; Girotto, G.; Goel, A.; Gögele, M.; Goodarzi, M. O; Graff, M.; Granot-Hershkovitz, E.; Grodstein, F.; Guarrera, S.; Gudbjartsson, D. F; Guity, K.; Gunnarsson, B.; Guo, Y.; Hagenaars, S. P; Haiman, C. A; Halevy, A.; Harris, T. B; Hedayati, M.; van Heel, D. A; Hirata, M.; Höfer, I.; Hsiung, C. A.; Huang, J.; Hung, Y.; Ikram, M A.; Jagadeesan, A.; Jousilahti, P.; Kamatani, Y.; Kanai, M.; Kerrison, N. D; Kessler, T.; Khaw, K.; Khor, C. C.; de Kleijn, D. P V; Koh, W.; Kolcic, I.; Kraft, P.; Krämer, B. K; Kutalik, Z.; Kuusisto, J.; Langenberg, C.; Launer, L. J; Lawlor, D. A; Lee, I.; Lee, W.; Lerch, M. M; Li, L.; Liu, J.; Loh, M.; London, S. J; Loomis, S.; Lu, Y.; Luan, J.; Mägi, R.; Manichaikul, A. W; Manunta, P.; Másson, G.; Matoba, N.; Mei, X. W; Meisinger, C.; Meitinger, T.; Mezzavilla, M.; Milani, L.; Millwood, I. Y; Momozawa, Y.; Moore, A.; Morange, P.; Moreno-Macias, H.; Mori, T. A; Morrison, A. C; Muka, T.; Murakami, Y.; Murray, A. D; de Mutsert, R.; Mychaleckyj, J. C; Nalls, M. A; Nauck, M.; Neville, M. J; Nolte, I. M; Ong, K. K; Orozco, L.; Padmanabhan, S.; Pálsson, G.; Pankow, J. S; Pattaro, C.; Pattie, A.; Polasek, O.; Poulter, N.; Pramstaller, P. P; Quintana-Murci, L.; Räikkönen, K.; Ralhan, S.; Rao, D. C; van Rheenen, W.; Rich, S. S; Ridker, P. M; Rietveld, C. A; Robino, A.; van Rooij, F. J A; Ruggiero, D.; Saba, Y.; Sabanayagam, C.; Sabater-Lleal, M.; Sala, C. F.; Salomaa, V.; Sandow, K.; Schmidt, H.; Scott, L. J; Scott, W. R; Sedaghati-Khayat, B.; Sennblad, B.; van Setten, J.; Sever, P. J; Sheu, W. H.; Shi, Y.; Shrestha, S.; Shukla, S. R.; Sigurdsson, J. K; Sikka, T. T.; Singh, J. R.; Smith, B. H; Stančáková, A.; Stanton, A.; Starr, J. M; Stefansdottir, L.; Straker, L.; Sulem, P.; Sveinbjornsson, G.; Swertz, M. A; Taylor, A. M; Taylor, K. D; Terzikhan, N.; Tham, Y.; Thorleifsson, G.; Thorsteinsdottir, U.; Tillander, A.; Tracy, R. P; Tusié-Luna, T.; Tzoulaki, I.; Vaccargiu, S.; Vangipurapu, J.; Veldink, J. H; Vitart, V.; Völker, U.; Vuoksimaa, E.; Wakil, S. M; Waldenberger, M.; Wander, G. S; Wang, Y. X.; Wareham, N. J; Wild, S.; Yajnik, C. S; Yuan, J.; Zeng, L.; Zhang, L.; Zhou, J.; Amin, N.; Asselbergs, F. W; Bakker, S. J L; Becker, D. M; Lehne, B.; Bennett, D. A; van den Berg, L. H; Berndt, S. I; Bharadwaj, D.; Bielak, L. F; Bochud, M.; Boehnke, M.; Bouchard, C.; Bradfield, J. P; Brody, J. A; Campbell, A.; Carmi, S.; Caulfield, M. J; Cesarini, D.; Chambers, J. C; Chandak, G. R.; Cheng, C.; Ciullo, M.; Cornelis, M.; Cusi, D.; Smith, G. D.; Deary, I. J; Dorajoo, R.; van Duijn, C. M; Ellinghaus, D.; Erdmann, J.; Eriksson, J. G; Evangelou, E.; Evans, M. K; Faul, J. D; Feenstra, B.; Feitosa, M.; Foisy, S.; Franke, A.; Friedlander, Y.; Gasparini, P.; Gieger, C.; Gonzalez, C.; Goyette, P.; Grant, S. F A; Griffiths, L. R; Groop, L.; Gudnason, V.; Gyllensten, U.; Hakonarson, H.; Hamsten, A.; van der Harst, P.; Heng, C.; Hicks, A. A; Hochner, H.; Huikuri, H.; Hunt, S. C; Jaddoe, V. W V; De Jager, P. L; Johannesson, M.; Johansson, A.; Jonas, J. B; Jukema, J W.; Junttila, J.; Kaprio, J.; Kardia, S. L R; Karpe, F.; Kumari, M.; Laakso, M.; van der Laan, S. W; Lahti, J.; Laudes, M.; Lea, R. A; Lieb, W.; Lumley, T.; Martin, N. G; März, W.; Matullo, G.; McCarthy, M. I; Medland, S. E; Merriman, T. R; Metspalu, A.; Meyer, B. F; Mohlke, K. L; Montgomery, G. W; Mook-Kanamori, D.; Munroe, P. B; North, K. E; Nyholt, D. R; O’Connell, J. R; Ober, C.; Oldehinkel, A. J; Palmas, W.; Palmer, C.; Pasterkamp, G. G; Patin, E.; Pennell, C. E; Perusse, L.; Peyser, P. A; Pirastu, M.; Polderman, T. J C; Porteous, D. J; Posthuma, D.; Psaty, B. M; Rioux, J. D; Rivadeneira, F.; Rotimi, C.; Rotter, J. I; Rudan, I.; den Ruijter, H. M; Sanghera, D. K; Sattar, N.; Schmidt, R.; Schulze, M. B; Schunkert, H.; Scott, R. A; Shuldiner, A. R; Sim, X.; Small, N.; Smith, J. A; Sotoodehnia, N.; Tai, E.; Teumer, A.; Timpson, N. J; Toniolo, D.; Trégouët, D.; Tuomi, T.; Vollenweider, P.; Wang, C. A; Weir, D. R; Whitfield, J. B; Wijmenga, C.; Wong, T.; Wright, J.; Yang, J.; Yu, L.; Zemel, B. S; Zonderman, A. B; Perola, M.; Magnusson, P. K E; Uitterlinden, A. G; Kooner, J. S; Chasman, D. I; Loos, R. J F; Franceschini, N.; Franke, L.; Haley, C. S; Hayward, C.; Walters, R. G; Perry, J. R B; Esko, T.; Helgason, A.; Stefansson, K.; Joshi, P. K; Kubo, M.; and Wilson, J. F\n\n\n \n \n \n \n Associations of autozygosity with a broad range of human phenotypes.\n \n \n \n\n\n \n\n\n\n Nat Commun, 10: 4957. October 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{clark_associations_2019,\n\ttitle = {Associations of autozygosity with a broad range of human phenotypes.},\n\tvolume = {10},\n\tissn = {2041-1723},\n\tdoi = {10.1038/s41467-019-12283-6},\n\tabstract = {{\\textless}p{\\textgreater}In many species, the offspring of related parents suffer reduced reproductive success, a phenomenon known as inbreeding depression. In humans, the importance of this effect has remained unclear, partly because reproduction between close relatives is both rare and frequently associated with confounding social factors. Here, using genomic inbreeding coefficients (F) for {\\textgreater}1.4 million individuals, we show that F is significantly associated (p {\\textless} 0.0005) with apparently deleterious changes in 32 out of 100 traits analysed. These changes are associated with runs of homozygosity (ROH), but not with common variant homozygosity, suggesting that genetic variants associated with inbreeding depression are predominantly rare. The effect on fertility is striking: F equivalent to the offspring of first cousins is associated with a 55\\% decrease [95\\% CI 44-66\\%] in the odds of having children. Finally, the effects of F are confirmed within full-sibling pairs, where the variation in F is independent of all environmental confounding.{\\textless}/p{\\textgreater}},\n\tjournal = {Nat Commun},\n\tauthor = {Clark, David W and Okada, Yukinori and Moore, Kristjan H S and Mason, Dan and Pirastu, Nicola and Gandin, Ilaria and Mattsson, Hannele and Barnes, Catriona L K and Lin, Kuang and Zhao, Jing Hua and Deelen, Patrick and Rohde, Rebecca and Schurmann, Claudia and Guo, Xiuqing and Giulianini, Franco and Zhang, Weihua and Medina-Gómez, Carolina and Karlsson, Robert and Bao, Yanchun and Bartz, Traci M and Baumbach, Clemens and Biino, Ginevra and Bixley, Matthew J and Brumat, Marco and Chai, Jin-Fang and Corre, Tanguy and Cousminer, Diana L and Dekker, Annelot M and Eccles, David A and van Eijk, Kristel R and Fuchsberger, Christian and Gao, He and Germain, Marine and Gordon, Scott D and de Haan, Hugoline G and Harris, Sarah E and Hofer, Edith and Huerta-Chagoya, Alicia and Igartua, Catherine and Jansen, Iris E and Jia, Yucheng and Kacprowski, Tim and Karlsson, Torgny and Kleber, Marcus E and Li, Shengchao Alfred and Li-Gao, Ruifang and Mahajan, Anubha and Matsuda, Koichi and Meidtner, Karina and Meng, Weihua and Montasser, May E and van der Most, Peter J and Munz, Matthias and Nutile, Teresa and Palviainen, Teemu and Prasad, Gauri and Prasad, Rashmi B and Priyanka, Tallapragada Divya Sri and Rizzi, Federica and Salvi, Erika and Sapkota, Bishwa R and Shriner, Daniel and Skotte, Line and Smart, Melissa C and Smith, Albert Vernon and van der Spek, Ashley and Spracklen, Cassandra N and Strawbridge, Rona J and Tajuddin, Salman M and Trompet, Stella and Turman, Constance and Verweij, Niek and Viberti, Clara and Wang, Lihua and Warren, Helen R and Wootton, Robyn E and Yanek, Lisa R and Yao, Jie and Yousri, Noha A and Zhao, Wei and Adeyemo, Adebowale A and Afaq, Saima and Aguilar-Salinas, Carlos Alberto and Akiyama, Masato and Albert, Matthew L and Allison, Matthew A and Alver, Maris and Aung, Tin and Azizi, Fereidoun and Bentley, Amy R and Boeing, Heiner and Boerwinkle, Eric and Borja, Judith B and de Borst, Gert J and Bottinger, Erwin P and Broer, Linda and Campbell, Harry and Chanock, Stephen and Chee, Miao-Li and Chen, Guanjie and Chen, Yii-der I and Chen, Zhengming and Chiu, Yen-Feng and Cocca, Massimiliano and Collins, Francis S and Concas, Maria Pina and Corley, Janie and Cugliari, Giovanni and van Dam, Rob M and Damulina, Anna and Daneshpour, Maryam S and Day, Felix R and Delgado, Graciela E and Dhana, Klodian and Doney, Alexander S F and Dörr, Marcus and Doumatey, Ayo P and Dzimiri, Nduna and Ebenesersdóttir, S Sunna and Elliott, Joshua and Elliott, Paul and Ewert, Ralf and Felix, Janine F and Fischer, Krista and Freedman, Barry I and Girotto, Giorgia and Goel, Anuj and Gögele, Martin and Goodarzi, Mark O and Graff, Mariaelisa and Granot-Hershkovitz, Einat and Grodstein, Francine and Guarrera, Simonetta and Gudbjartsson, Daniel F and Guity, Kamran and Gunnarsson, Bjarni and Guo, Yu and Hagenaars, Saskia P and Haiman, Christopher A and Halevy, Avner and Harris, Tamara B and Hedayati, Mehdi and van Heel, David A and Hirata, Makoto and Höfer, Imo and Hsiung, Chao Agnes and Huang, Jinyan and Hung, Yi-Jen and Ikram, M Arfan and Jagadeesan, Anuradha and Jousilahti, Pekka and Kamatani, Yoichiro and Kanai, Masahiro and Kerrison, Nicola D and Kessler, Thorsten and Khaw, Kay-Tee and Khor, Chiea Chuen and de Kleijn, Dominique P V and Koh, Woon-Puay and Kolcic, Ivana and Kraft, Peter and Krämer, Bernhard K and Kutalik, Zoltán and Kuusisto, Johanna and Langenberg, Claudia and Launer, Lenore J and Lawlor, Deborah A and Lee, I-Te and Lee, Wen-Jane and Lerch, Markus M and Li, Liming and Liu, Jianjun and Loh, Marie and London, Stephanie J and Loomis, Stephanie and Lu, Yingchang and Luan, Jian’an and Mägi, Reedik and Manichaikul, Ani W and Manunta, Paolo and Másson, Gísli and Matoba, Nana and Mei, Xue W and Meisinger, Christa and Meitinger, Thomas and Mezzavilla, Massimo and Milani, Lili and Millwood, Iona Y and Momozawa, Yukihide and Moore, Amy and Morange, Pierre-Emmanuel and Moreno-Macias, Hortensia and Mori, Trevor A and Morrison, Alanna C and Muka, Taulant and Murakami, Yoshinori and Murray, Alison D and de Mutsert, Renée and Mychaleckyj, Josyf C and Nalls, Mike A and Nauck, Matthias and Neville, Matt J and Nolte, Ilja M and Ong, Ken K and Orozco, Lorena and Padmanabhan, Sandosh and Pálsson, Gunnar and Pankow, James S and Pattaro, Cristian and Pattie, Alison and Polasek, Ozren and Poulter, Neil and Pramstaller, Peter P and Quintana-Murci, Lluis and Räikkönen, Katri and Ralhan, Sarju and Rao, Dabeeru C and van Rheenen, Wouter and Rich, Stephen S and Ridker, Paul M and Rietveld, Cornelius A and Robino, Antonietta and van Rooij, Frank J A and Ruggiero, Daniela and Saba, Yasaman and Sabanayagam, Charumathi and Sabater-Lleal, Maria and Sala, Cinzia Felicita and Salomaa, Veikko and Sandow, Kevin and Schmidt, Helena and Scott, Laura J and Scott, William R and Sedaghati-Khayat, Bahareh and Sennblad, Bengt and van Setten, Jessica and Sever, Peter J and Sheu, Wayne H-H and Shi, Yuan and Shrestha, Smeeta and Shukla, Sharvari Rahul and Sigurdsson, Jon K and Sikka, Timo Tonis and Singh, Jai Rup and Smith, Blair H and Stančáková, Alena and Stanton, Alice and Starr, John M and Stefansdottir, Lilja and Straker, Leon and Sulem, Patrick and Sveinbjornsson, Gardar and Swertz, Morris A and Taylor, Adele M and Taylor, Kent D and Terzikhan, Natalie and Tham, Yih-Chung and Thorleifsson, Gudmar and Thorsteinsdottir, Unnur and Tillander, Annika and Tracy, Russell P and Tusié-Luna, Teresa and Tzoulaki, Ioanna and Vaccargiu, Simona and Vangipurapu, Jagadish and Veldink, Jan H and Vitart, Veronique and Völker, Uwe and Vuoksimaa, Eero and Wakil, Salma M and Waldenberger, Melanie and Wander, Gurpreet S and Wang, Ya Xing and Wareham, Nicholas J and Wild, Sarah and Yajnik, Chittaranjan S and Yuan, Jian-Min and Zeng, Lingyao and Zhang, Liang and Zhou, Jie and Amin, Najaf and Asselbergs, Folkert W and Bakker, Stephan J L and Becker, Diane M and Lehne, Benjamin and Bennett, David A and van den Berg, Leonard H and Berndt, Sonja I and Bharadwaj, Dwaipayan and Bielak, Lawrence F and Bochud, Murielle and Boehnke, Mike and Bouchard, Claude and Bradfield, Jonathan P and Brody, Jennifer A and Campbell, Archie and Carmi, Shai and Caulfield, Mark J and Cesarini, David and Chambers, John C and Chandak, Giriraj Ratan and Cheng, Ching-Yu and Ciullo, Marina and Cornelis, Marilyn and Cusi, Daniele and Smith, George Davey and Deary, Ian J and Dorajoo, Rajkumar and van Duijn, Cornelia M and Ellinghaus, David and Erdmann, Jeanette and Eriksson, Johan G and Evangelou, Evangelos and Evans, Michele K and Faul, Jessica D and Feenstra, Bjarke and Feitosa, Mary and Foisy, Sylvain and Franke, Andre and Friedlander, Yechiel and Gasparini, Paolo and Gieger, Christian and Gonzalez, Clicerio and Goyette, Philippe and Grant, Struan F A and Griffiths, Lyn R and Groop, Leif and Gudnason, Vilmundur and Gyllensten, Ulf and Hakonarson, Hakon and Hamsten, Anders and van der Harst, Pim and Heng, Chew-Kiat and Hicks, Andrew A and Hochner, Hagit and Huikuri, Heikki and Hunt, Steven C and Jaddoe, Vincent W V and De Jager, Philip L and Johannesson, Magnus and Johansson, Asa and Jonas, Jost B and Jukema, J Wouter and Junttila, Juhani and Kaprio, Jaakko and Kardia, Sharon L R and Karpe, Fredrik and Kumari, Meena and Laakso, Markku and van der Laan, Sander W and Lahti, Jari and Laudes, Matthias and Lea, Rodney A and Lieb, Wolfgang and Lumley, Thomas and Martin, Nicholas G and März, Winfried and Matullo, Giuseppe and McCarthy, Mark I and Medland, Sarah E and Merriman, Tony R and Metspalu, Andres and Meyer, Brian F and Mohlke, Karen L and Montgomery, Grant W and Mook-Kanamori, Dennis and Munroe, Patricia B and North, Kari E and Nyholt, Dale R and O’Connell, Jeffery R and Ober, Carole and Oldehinkel, Albertine J and Palmas, Walter and Palmer, Colin and Pasterkamp, Gerard G and Patin, Etienne and Pennell, Craig E and Perusse, Louis and Peyser, Patricia A and Pirastu, Mario and Polderman, Tinca J C and Porteous, David J and Posthuma, Danielle and Psaty, Bruce M and Rioux, John D and Rivadeneira, Fernando and Rotimi, Charles and Rotter, Jerome I and Rudan, Igor and den Ruijter, Hester M and Sanghera, Dharambir K and Sattar, Naveed and Schmidt, Reinhold and Schulze, Matthias B and Schunkert, Heribert and Scott, Robert A and Shuldiner, Alan R and Sim, Xueling and Small, Neil and Smith, Jennifer A and Sotoodehnia, Nona and Tai, E-Shyong and Teumer, Alexander and Timpson, Nicholas J and Toniolo, Daniela and Trégouët, David-Alexandre and Tuomi, Tiinamaija and Vollenweider, Peter and Wang, Carol A and Weir, David R and Whitfield, John B and Wijmenga, Cisca and Wong, Tien-Yin and Wright, John and Yang, Jingyun and Yu, Lei and Zemel, Babette S and Zonderman, Alan B and Perola, Markus and Magnusson, Patrik K E and Uitterlinden, André G and Kooner, Jaspal S and Chasman, Daniel I and Loos, Ruth J F and Franceschini, Nora and Franke, Lude and Haley, Chris S and Hayward, Caroline and Walters, Robin G and Perry, John R B and Esko, Tõnu and Helgason, Agnar and Stefansson, Kari and Joshi, Peter K and Kubo, Michiaki and Wilson, James F},\n\tmonth = oct,\n\tyear = {2019},\n\tpages = {4957},\n}\n\n\n\n

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\n \n\n \n \n Mishra, A.; Chauhan, G.; Violleau, M.; Vojinovic, D.; Jian, X.; Bis, J. C; Li, S.; Saba, Y.; Grenier-Boley, B.; Yang, Q.; Bartz, T. M; Hofer, E.; Soumaré, A.; Peng, F.; Duperron, M.; Foglio, M.; Mosley, T. H; Schmidt, R.; Psaty, B. M; Launer, L. J; Boerwinkle, E.; Zhu, Y.; Mazoyer, B.; Lathrop, M.; Bellenguez, C.; van Duijn, C. M; Ikram, M A.; Schmidt, H.; Longstreth, W T; Fornage, M.; Seshadri, S.; Joutel, A.; Tzourio, C.; and Debette, S.\n\n\n \n \n \n \n Association of variants in HTRA1 and NOTCH3 with MRI-defined extremes of cerebral small vessel disease in older subjects.\n \n \n \n\n\n \n\n\n\n Brain. March 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{mishra_association_2019,\n\ttitle = {Association of variants in {HTRA1} and {NOTCH3} with {MRI}-defined extremes of cerebral small vessel disease in older subjects.},\n\tissn = {1460-2156},\n\tdoi = {10.1093/brain/awz024},\n\tabstract = {{\\textless}p{\\textgreater}We report a composite extreme phenotype design using distribution of white matter hyperintensities and brain infarcts in a population-based cohort of older persons for gene-mapping of cerebral small vessel disease. We demonstrate its application in the 3C-Dijon whole exome sequencing (WES) study (n = 1924, nWESextremes = 512), with both single variant and gene-based association tests. We used other population-based cohort studies participating in the CHARGE consortium for replication, using whole exome sequencing (nWES = 2,868, nWESextremes = 956) and genome-wide genotypes (nGW = 9924, nGWextremes = 3308). We restricted our study to candidate genes known to harbour mutations for Mendelian small vessel disease: NOTCH3, HTRA1, COL4A1, COL4A2 and TREX1. We identified significant associations of a common intronic variant in HTRA1, rs2293871 using single variant association testing (Pdiscovery = 8.21 × 10-5, Preplication = 5.25 × 10-3, Pcombined = 4.72 × 10-5) and of NOTCH3 using gene-based tests (Pdiscovery = 1.61 × 10-2, Preplication = 3.99 × 10-2, Pcombined = 5.31 × 10-3). Follow-up analysis identified significant association of rs2293871 with small vessel ischaemic stroke, and two blood expression quantitative trait loci of HTRA1 in linkage disequilibrium. Additionally, we identified two participants in the 3C-Dijon cohort (0.4\\%) carrying heterozygote genotypes at known pathogenic variants for familial small vessel disease within NOTCH3 and HTRA1. In conclusion, our proof-of-concept study provides strong evidence that using a novel composite MRI-derived phenotype for extremes of small vessel disease can facilitate the identification of genetic variants underlying small vessel disease, both common variants and those with rare and low frequency. The findings demonstrate shared mechanisms and a continuum between genes underlying Mendelian small vessel disease and those contributing to the common, multifactorial form of the disease.{\\textless}/p{\\textgreater}},\n\tjournal = {Brain},\n\tauthor = {Mishra, Aniket and Chauhan, Ganesh and Violleau, Marie-Helene and Vojinovic, Dina and Jian, Xueqiu and Bis, Joshua C and Li, Shuo and Saba, Yasaman and Grenier-Boley, Benjamin and Yang, Qiong and Bartz, Traci M and Hofer, Edith and Soumaré, Aïcha and Peng, Fen and Duperron, Marie-Gabrielle and Foglio, Mario and Mosley, Thomas H and Schmidt, Reinhold and Psaty, Bruce M and Launer, Lenore J and Boerwinkle, Eric and Zhu, Yicheng and Mazoyer, Bernard and Lathrop, Mark and Bellenguez, Céline and van Duijn, Cornelia M and Ikram, M Arfan and Schmidt, Helena and Longstreth, W T and Fornage, Myriam and Seshadri, Sudha and Joutel, Anne and Tzourio, Christophe and Debette, Stephanie},\n\tmonth = mar,\n\tyear = {2019},\n}\n\n\n\n

\n\n\n

\n \\textlessp\\textgreaterWe report a composite extreme phenotype design using distribution of white matter hyperintensities and brain infarcts in a population-based cohort of older persons for gene-mapping of cerebral small vessel disease. We demonstrate its application in the 3C-Dijon whole exome sequencing (WES) study (n = 1924, nWESextremes = 512), with both single variant and gene-based association tests. We used other population-based cohort studies participating in the CHARGE consortium for replication, using whole exome sequencing (nWES = 2,868, nWESextremes = 956) and genome-wide genotypes (nGW = 9924, nGWextremes = 3308). We restricted our study to candidate genes known to harbour mutations for Mendelian small vessel disease: NOTCH3, HTRA1, COL4A1, COL4A2 and TREX1. We identified significant associations of a common intronic variant in HTRA1, rs2293871 using single variant association testing (Pdiscovery = 8.21 × 10-5, Preplication = 5.25 × 10-3, Pcombined = 4.72 × 10-5) and of NOTCH3 using gene-based tests (Pdiscovery = 1.61 × 10-2, Preplication = 3.99 × 10-2, Pcombined = 5.31 × 10-3). Follow-up analysis identified significant association of rs2293871 with small vessel ischaemic stroke, and two blood expression quantitative trait loci of HTRA1 in linkage disequilibrium. Additionally, we identified two participants in the 3C-Dijon cohort (0.4%) carrying heterozygote genotypes at known pathogenic variants for familial small vessel disease within NOTCH3 and HTRA1. In conclusion, our proof-of-concept study provides strong evidence that using a novel composite MRI-derived phenotype for extremes of small vessel disease can facilitate the identification of genetic variants underlying small vessel disease, both common variants and those with rare and low frequency. The findings demonstrate shared mechanisms and a continuum between genes underlying Mendelian small vessel disease and those contributing to the common, multifactorial form of the disease.\\textless/p\\textgreater\n

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\n \n\n \n \n Steubl, D.; Bůzková, P.; Garimella, P. S; Ix, J. H; Devarajan, P.; Bennett, M. R; Chaves, P. H M; Shlipak, M. G; Bansal, N.; and Sarnak, M. J\n\n\n \n \n \n \n Association of serum uromodulin with mortality and cardiovascular disease in the elderly-the Cardiovascular Health Study.\n \n \n \n\n\n \n\n\n\n Nephrol Dial Transplant. March 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{steubl_association_2019,\n\ttitle = {Association of serum uromodulin with mortality and cardiovascular disease in the elderly-the {Cardiovascular} {Health} {Study}.},\n\tissn = {1460-2385},\n\tdoi = {10.1093/ndt/gfz008},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{BACKGROUND: }Uromodulin (UMOD) is released by renal tubular cells into the serum (sUMOD) and urine. Lower urine UMOD has been linked to mortality and cardiovascular disease but much less is known about sUMOD. We evaluated the association of sUMOD with these outcomes in community-dwelling older adults.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS: }We measured sUMOD in a random subcohort of 933 participants enrolled in the Cardiovascular Health Study. The associations of sUMOD with all-cause mortality, incident heart failure (HF) and incident cardiovascular disease (CVD; myocardial infarction, stroke and mortality due to coronary disease or stroke) were evaluated using multivariable Cox regression, adjusting for study participants’ demographics, estimated glomerular filtration rate (eGFR), albuminuria and CVD risk factors. Generalized additive models with splines were used to address the functional form of sUMOD with outcomes. Due to nonlinear associations of sUMOD with all outcomes, 2.5\\% of the values on either end of the sUMOD distribution were excluded from the analyses, limiting the range of sUMOD to 34.3-267.1 ng/mL.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{RESULTS: }The mean age was 78 ± 5 years, 40\\% were male, sUMOD level was 127 ± 64 ng/mL, eGFR was 63 mL/min/1.73 m2 and 42\\% had CKD defined as eGFR {\\textless}60 mL/min/1.73 m2. Patients in the lower sUMOD quartiles had lower eGFR and higher albuminuria (P {\\textless} 0.01, respectively). During a median follow-up of 9.9 years, 805 patients died, 283 developed HF and 274 developed CVD. In multivariable analysis, higher sUMOD was significantly associated with a lower hazard for mortality hazard ratio [HR] 0.89 [95\\% confidence interval (CI) 0.80-0.99] per 1 standard deviation (SD) higher sUMOD, CVD [HR 0.80 (95\\% CI 0.67-0.96)] and the composite endpoint [HR 0.88 (95\\% CI 0.78-0.99)]; the association with HF was not statistically significant [HR 0.84 (95\\% CI 0.70-1.01)].{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSION: }Higher sUMOD is independently associated with a lower risk for mortality and CVD in older adults.{\\textless}/p{\\textgreater}},\n\tjournal = {Nephrol Dial Transplant},\n\tauthor = {Steubl, Dominik and Bůzková, Petra and Garimella, Pranav S and Ix, Joachim H and Devarajan, Prasad and Bennett, Michael R and Chaves, Paulo H M and Shlipak, Michael G and Bansal, Nisha and Sarnak, Mark J},\n\tmonth = mar,\n\tyear = {2019},\n}\n\n\n\n

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\n \\textlessp\\textgreater\\textbfBACKGROUND: Uromodulin (UMOD) is released by renal tubular cells into the serum (sUMOD) and urine. Lower urine UMOD has been linked to mortality and cardiovascular disease but much less is known about sUMOD. We evaluated the association of sUMOD with these outcomes in community-dwelling older adults.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfMETHODS: We measured sUMOD in a random subcohort of 933 participants enrolled in the Cardiovascular Health Study. The associations of sUMOD with all-cause mortality, incident heart failure (HF) and incident cardiovascular disease (CVD; myocardial infarction, stroke and mortality due to coronary disease or stroke) were evaluated using multivariable Cox regression, adjusting for study participants’ demographics, estimated glomerular filtration rate (eGFR), albuminuria and CVD risk factors. Generalized additive models with splines were used to address the functional form of sUMOD with outcomes. Due to nonlinear associations of sUMOD with all outcomes, 2.5% of the values on either end of the sUMOD distribution were excluded from the analyses, limiting the range of sUMOD to 34.3-267.1 ng/mL.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfRESULTS: The mean age was 78 ± 5 years, 40% were male, sUMOD level was 127 ± 64 ng/mL, eGFR was 63 mL/min/1.73 m2 and 42% had CKD defined as eGFR \\textless60 mL/min/1.73 m2. Patients in the lower sUMOD quartiles had lower eGFR and higher albuminuria (P \\textless 0.01, respectively). During a median follow-up of 9.9 years, 805 patients died, 283 developed HF and 274 developed CVD. In multivariable analysis, higher sUMOD was significantly associated with a lower hazard for mortality hazard ratio [HR] 0.89 [95% confidence interval (CI) 0.80-0.99] per 1 standard deviation (SD) higher sUMOD, CVD [HR 0.80 (95% CI 0.67-0.96)] and the composite endpoint [HR 0.88 (95% CI 0.78-0.99)]; the association with HF was not statistically significant [HR 0.84 (95% CI 0.70-1.01)].\\textless/p\\textgreater\\textlessp\\textgreater\\textbfCONCLUSION: Higher sUMOD is independently associated with a lower risk for mortality and CVD in older adults.\\textless/p\\textgreater\n

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\n \n\n \n \n Carbone, L. D; Bůzková, P.; Fink, H. A; Raiford, M.; Le, B.; Isales, C. M; Shikany, J. M; Coughlin, S. S; and Robbins, J. A\n\n\n \n \n \n \n Association of Dietary Niacin Intake With Incident Hip Fracture, BMD, and Body Composition: The Cardiovascular Health Study.\n \n \n \n\n\n \n\n\n\n J Bone Miner Res. January 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{carbone_association_2019,\n\ttitle = {Association of {Dietary} {Niacin} {Intake} {With} {Incident} {Hip} {Fracture}, {BMD}, and {Body} {Composition}: {The} {Cardiovascular} {Health} {Study}.},\n\tissn = {1523-4681},\n\tdoi = {10.1002/jbmr.3639},\n\tabstract = {{\\textless}p{\\textgreater}Interest in niacin has increased in the setting of reports suggesting that niacin plays a role in diseases of aging. No study to date has examined the association of dietary niacin intake with multiple skeletal health parameters including bone mineral density (BMD), hip fractures, and body composition, and none have included both African American and white men and women. Participants included 5187 men and women {\\textgreater}=65 years from the Cardiovascular Health Study (CHS). Mean daily dietary niacin intake was 32.6 mg, with quartiles 1 through 4 defined as 3.6 to 21.8 mg/day, 21.9 to 30.2 mg/day, 30.3 to 40.9 mg/day, and 41.0 to 102.4 mg/day, respectively. Risk of incident hip fracture per 10 mg increment of daily dietary niacin intake was estimated using proportional hazards models. During a median follow-up of 13 years, 725 participants had an incident hip fracture. In models adjusted for demographic and clinical characteristics and diet, dietary niacin intake was significantly associated with an increased risk of hip fractures (hazard ratio [HR] 1.12; 95\\% CI, 1.01 to 1.24) with spline models suggesting a U-shaped association. In post hoc analyses, both the lowest (HR 1.31; 95\\% CI, 1.04 to 1.66) and highest (HR 1.53; 95\\% CI, 1.20 to 1.95) quartiles of niacin intake were associated with an increased risk of incident hip fracture versus quartiles 2 and 3. There was a trend for a significant inverse association of dietary niacin intake with hip BMD (p = 0.06), but no significant association with total body BMD or any body composition measures. In this cohort of elderly, community-dwelling African American and white men and women, both high and low dietary niacin intakes were associated with a significantly increased risk of subsequent hip fracture, suggesting a possible U-shaped association. By comparison, dietary niacin may have an inverse linear association with hip BMD. © 2018 American Society for Bone and Mineral Research.{\\textless}/p{\\textgreater}},\n\tjournal = {J Bone Miner Res},\n\tauthor = {Carbone, Laura D and Bůzková, Petra and Fink, Howard A and Raiford, Mattie and Le, Brian and Isales, Carlos M and Shikany, James M and Coughlin, Steven S and Robbins, John A},\n\tmonth = jan,\n\tyear = {2019},\n}\n\n\n\n

\n\n\n

\n \\textlessp\\textgreaterInterest in niacin has increased in the setting of reports suggesting that niacin plays a role in diseases of aging. No study to date has examined the association of dietary niacin intake with multiple skeletal health parameters including bone mineral density (BMD), hip fractures, and body composition, and none have included both African American and white men and women. Participants included 5187 men and women \\textgreater=65 years from the Cardiovascular Health Study (CHS). Mean daily dietary niacin intake was 32.6 mg, with quartiles 1 through 4 defined as 3.6 to 21.8 mg/day, 21.9 to 30.2 mg/day, 30.3 to 40.9 mg/day, and 41.0 to 102.4 mg/day, respectively. Risk of incident hip fracture per 10 mg increment of daily dietary niacin intake was estimated using proportional hazards models. During a median follow-up of 13 years, 725 participants had an incident hip fracture. In models adjusted for demographic and clinical characteristics and diet, dietary niacin intake was significantly associated with an increased risk of hip fractures (hazard ratio [HR] 1.12; 95% CI, 1.01 to 1.24) with spline models suggesting a U-shaped association. In post hoc analyses, both the lowest (HR 1.31; 95% CI, 1.04 to 1.66) and highest (HR 1.53; 95% CI, 1.20 to 1.95) quartiles of niacin intake were associated with an increased risk of incident hip fracture versus quartiles 2 and 3. There was a trend for a significant inverse association of dietary niacin intake with hip BMD (p = 0.06), but no significant association with total body BMD or any body composition measures. In this cohort of elderly, community-dwelling African American and white men and women, both high and low dietary niacin intakes were associated with a significantly increased risk of subsequent hip fracture, suggesting a possible U-shaped association. By comparison, dietary niacin may have an inverse linear association with hip BMD. © 2018 American Society for Bone and Mineral Research.\\textless/p\\textgreater\n

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\n \n\n \n \n Le, B.; Bůzková, P.; Robbins, J. A; Fink, H. A; Raiford, M.; Isales, C. M; Shikany, J. M; Coughlin, S. S; and Carbone, L. D\n\n\n \n \n \n \n The Association of Aromatic Amino Acids with Incident Hip Fracture, aBMD, and Body Composition from the Cardiovascular Health Study.\n \n \n \n\n\n \n\n\n\n Calcif Tissue Int, 105: 161–172. August 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{le_association_2019,\n\ttitle = {The {Association} of {Aromatic} {Amino} {Acids} with {Incident} {Hip} {Fracture}, {aBMD}, and {Body} {Composition} from the {Cardiovascular} {Health} {Study}.},\n\tvolume = {105},\n\tissn = {1432-0827},\n\tdoi = {10.1007/s00223-019-00562-9},\n\tabstract = {{\\textless}p{\\textgreater}In 5187 persons from the Cardiovascular Health Study, there was no significant association of dietary intakes of aromatic amino acids (AAA) with areal BMD of the hip or body composition. However, those who had the lowest dietary intakes of AAA were at increased risk for incident hip fractures. Prior studies of the association of protein intake with osteoporosis are conflicting and have not directly examined the relationship of aromatic amino acids (AAA) with fractures, areal bone mineral density (aBMD), and body composition. We sought to determine the relationship of dietary intakes of AAA with osteoporosis parameters in elderly men and women. 5187 men and women aged {\\textgreater}= 65 years from the Cardiovascular Health Study (CHS) with dietary intakes of AAA (tryptophan, phenylalanine, tyrosine) estimated by food frequency questionnaire (FFQ) were included. We examined the relationship between a one-time estimate of daily dietary AAA intake with risk of incident hip fractures over a median of 13.2 years of fracture follow-up. A subset (n = 1336) who had dual energy X-ray absorptiometry (DXA) performed were included in a cross-sectional analysis of the association of dietary AAA intake with aBMD of the total hip and measurements of body composition. In multivariable models adjusted for demographic and clinical variables, medication use, and diet, higher dietary AAA intake was not significantly associated with incident hip fractures. All hazard ratios (HR) were less than one (tryptophan, HR 0.14, 95\\% CI 0.01 to 1.89; phenylalanine, HR 0.60, 95\\% CI 0.23 to 1.55; tyrosine, HR 0.59, 95\\% CI 0.27 to 1.32), but confidence intervals were wide and included no difference. However, in post hoc analyses, the lowest quartile of intake for each AAA was associated with an increased risk for hip fracture compared to higher quartiles (p {\\textless}= 0.047 for all). Dietary AAA intakes were not significantly associated with total hip aBMD or any measurements of body composition. Overall, there was no significant association of dietary AAA intake with hip fractures, aBMD of the hip, or body composition. However, there may be a subset of elderly individuals with low dietary intakes of AAA who are at increased for hip fractures.{\\textless}/p{\\textgreater}},\n\tjournal = {Calcif Tissue Int},\n\tauthor = {Le, Brian and Bůzková, Petra and Robbins, John A and Fink, Howard A and Raiford, Mattie and Isales, Carlos M and Shikany, James M and Coughlin, Steven S and Carbone, Laura D},\n\tmonth = aug,\n\tyear = {2019},\n\tpages = {161--172},\n}\n\n\n\n

\n\n\n

\n \\textlessp\\textgreaterIn 5187 persons from the Cardiovascular Health Study, there was no significant association of dietary intakes of aromatic amino acids (AAA) with areal BMD of the hip or body composition. However, those who had the lowest dietary intakes of AAA were at increased risk for incident hip fractures. Prior studies of the association of protein intake with osteoporosis are conflicting and have not directly examined the relationship of aromatic amino acids (AAA) with fractures, areal bone mineral density (aBMD), and body composition. We sought to determine the relationship of dietary intakes of AAA with osteoporosis parameters in elderly men and women. 5187 men and women aged \\textgreater= 65 years from the Cardiovascular Health Study (CHS) with dietary intakes of AAA (tryptophan, phenylalanine, tyrosine) estimated by food frequency questionnaire (FFQ) were included. We examined the relationship between a one-time estimate of daily dietary AAA intake with risk of incident hip fractures over a median of 13.2 years of fracture follow-up. A subset (n = 1336) who had dual energy X-ray absorptiometry (DXA) performed were included in a cross-sectional analysis of the association of dietary AAA intake with aBMD of the total hip and measurements of body composition. In multivariable models adjusted for demographic and clinical variables, medication use, and diet, higher dietary AAA intake was not significantly associated with incident hip fractures. All hazard ratios (HR) were less than one (tryptophan, HR 0.14, 95% CI 0.01 to 1.89; phenylalanine, HR 0.60, 95% CI 0.23 to 1.55; tyrosine, HR 0.59, 95% CI 0.27 to 1.32), but confidence intervals were wide and included no difference. However, in post hoc analyses, the lowest quartile of intake for each AAA was associated with an increased risk for hip fracture compared to higher quartiles (p \\textless= 0.047 for all). Dietary AAA intakes were not significantly associated with total hip aBMD or any measurements of body composition. Overall, there was no significant association of dietary AAA intake with hip fractures, aBMD of the hip, or body composition. However, there may be a subset of elderly individuals with low dietary intakes of AAA who are at increased for hip fractures.\\textless/p\\textgreater\n

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\n \n\n \n \n Karunananthan, S.; Moodie, E. E M; Bergman, H.; Payette, H.; Wolfson, D.; Diehr, P. H; and Wolfson, C.\n\n\n \n \n \n \n The association between physical function and proximity to death in older adults: a multilevel analysis of 4,150 decedents from the Cardiovascular Health Study.\n \n \n \n\n\n \n\n\n\n Ann Epidemiol, 35: 59–65.e5. July 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{karunananthan_association_2019,\n\ttitle = {The association between physical function and proximity to death in older adults: a multilevel analysis of 4,150 decedents from the {Cardiovascular} {Health} {Study}.},\n\tvolume = {35},\n\tissn = {1873-2585},\n\tdoi = {10.1016/j.annepidem.2019.04.005},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{PURPOSE: }When examining whether poor physical function is a risk factor for imminent death in older adults, one challenge is the lack of a meaningful time origin, a time point on which the estimate of time-to-death is anchored. In this study, we overcame this challenge by discarding the traditional-and flawed-approach of survival analysis with "time since beginning of follow up" as the time variable, and instead used a novel analytic approach that uses time-to-death as a covariate to examine its association with physical function.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS: }Physical function and other covariates were measured annually in the Cardiovascular Health Study on 4150 individuals followed up to their time of death. Using multilevel models, we estimated gait speed and grip strength in relation to two time axes: age and proximity to death.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{RESULTS: }As individuals approached death, both gait speed and grip strength decreased significantly. However, after adjustment for health and lifestyle covariates, there was significant variation in the level of physical function between individuals.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSION: }Although physical function was significantly associated with time-to-death, there was significant variation in level of physical function between individuals at comparable proximity to death. A better understanding of these variations is needed before measures of physical function are recommended as a clinical tool for identifying individuals at high risk of death.{\\textless}/p{\\textgreater}},\n\tjournal = {Ann Epidemiol},\n\tauthor = {Karunananthan, Sathya and Moodie, Erica E M and Bergman, Howard and Payette, Hélène and Wolfson, David and Diehr, Paula H and Wolfson, Christina},\n\tmonth = jul,\n\tyear = {2019},\n\tpages = {59--65.e5},\n}\n\n\n\n

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\n \n\n \n \n Bůžková, P; Barzilay, J I; and Mukamal, K J\n\n\n \n \n \n \n Assessing risk factors of non-fatal outcomes amid a competing risk of mortality: the example of hip fracture.\n \n \n \n\n\n \n\n\n\n Osteoporos Int. June 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{buzkova_assessing_2019,\n\ttitle = {Assessing risk factors of non-fatal outcomes amid a competing risk of mortality: the example of hip fracture.},\n\tissn = {1433-2965},\n\tdoi = {10.1007/s00198-019-05048-w},\n\tabstract = {{\\textless}p{\\textgreater}The Fine-Gray method is often used instead of Cox regression to account for competing risks of death in time-to-event analyses for non-fatal outcomes. A series of examples using well-known risk factors of hip fracture in an older cohort with substantial competing mortality demonstrates that the Fine-Gray approach can yield estimates that implausibly contradict long-established associations, while Cox regression preserves them. Cox regression is generally preferred for risk factor-outcome associations even in the presence of competing risk of death.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{INTRODUCTION: }Factors like age, sex, and race are associated not only with risk of hip fracture but also with mortality. Substantial misunderstanding remains regarding the appropriate statistical approach to account for the competing risk of mortality.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS: }In the Cardiovascular Health Study, an ongoing cohort study of 5888 older adults, we followed participants for incident hip fracture from their 1992-1993 visit through June 2014. We contrasted the conventional cause-specific Cox analysis, which censors individuals at the time of death, with the Fine-Gray (FG) approach, which extends participant follow-up even after death, to estimate the association of well-established demographic and clinical factors with incident hip fracture.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{RESULTS: }For age, current smoking and sex, Cox and FG methods yielded directionally concordant but quantitatively different strengths of association. For example, the Cox hazard ratio (HR) for a 5-year increment in age was 1.74 (95\\% CI, 1.61-1.87), while the corresponding FG HR was 1.16 (1.09-1.24). In contrast, the FG approach estimated a stronger association of hip fracture with sex. The two approaches yielded nearly identical results for race. For diabetes and kidney function, the estimates were discordant in direction, and the FG HRs suggested effects that were in the opposite direction of well-understood and widely accepted associations.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSIONS: }Cause-specific Cox models provide appropriate estimates of hazard for non-fatal outcomes like hip fracture even in the presence of competing risk of mortality. The Cox approach estimates hazard in the population of individuals who have not yet had an incident hip fracture and remain alive, which is typically the group of clinical interest. The Fine-Gray method estimates hazard in a hypothetical population that can yield misleading inferences about risk factors in populations of clinical interest.{\\textless}/p{\\textgreater}},\n\tjournal = {Osteoporos Int},\n\tauthor = {Bůžková, P and Barzilay, J I and Mukamal, K J},\n\tmonth = jun,\n\tyear = {2019},\n}\n\n\n\n

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\n \\textlessp\\textgreaterThe Fine-Gray method is often used instead of Cox regression to account for competing risks of death in time-to-event analyses for non-fatal outcomes. A series of examples using well-known risk factors of hip fracture in an older cohort with substantial competing mortality demonstrates that the Fine-Gray approach can yield estimates that implausibly contradict long-established associations, while Cox regression preserves them. Cox regression is generally preferred for risk factor-outcome associations even in the presence of competing risk of death.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfINTRODUCTION: Factors like age, sex, and race are associated not only with risk of hip fracture but also with mortality. Substantial misunderstanding remains regarding the appropriate statistical approach to account for the competing risk of mortality.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfMETHODS: In the Cardiovascular Health Study, an ongoing cohort study of 5888 older adults, we followed participants for incident hip fracture from their 1992-1993 visit through June 2014. We contrasted the conventional cause-specific Cox analysis, which censors individuals at the time of death, with the Fine-Gray (FG) approach, which extends participant follow-up even after death, to estimate the association of well-established demographic and clinical factors with incident hip fracture.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfRESULTS: For age, current smoking and sex, Cox and FG methods yielded directionally concordant but quantitatively different strengths of association. For example, the Cox hazard ratio (HR) for a 5-year increment in age was 1.74 (95% CI, 1.61-1.87), while the corresponding FG HR was 1.16 (1.09-1.24). In contrast, the FG approach estimated a stronger association of hip fracture with sex. The two approaches yielded nearly identical results for race. For diabetes and kidney function, the estimates were discordant in direction, and the FG HRs suggested effects that were in the opposite direction of well-understood and widely accepted associations.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfCONCLUSIONS: Cause-specific Cox models provide appropriate estimates of hazard for non-fatal outcomes like hip fracture even in the presence of competing risk of mortality. The Cox approach estimates hazard in the population of individuals who have not yet had an incident hip fracture and remain alive, which is typically the group of clinical interest. The Fine-Gray method estimates hazard in a hypothetical population that can yield misleading inferences about risk factors in populations of clinical interest.\\textless/p\\textgreater\n

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\n \n\n \n \n Oelsner, E. C; Balte, P. P; Grams, M. E; Cassano, P. A; Jacobs, D. R; Barr, R G.; Burkart, K. M; Kalhan, R.; Kronmal, R.; Loehr, L. R; O’Connor, G. T; Schwartz, J. E; Shlipak, M.; Tracy, R. P; Tsai, M. Y; White, W.; and Yende, S.\n\n\n \n \n \n \n Albuminuria, Lung Function Decline, and Risk of Incident Chronic Obstructive Pulmonary Disease. The NHLBI Pooled Cohorts Study.\n \n \n \n\n\n \n\n\n\n Am J Respir Crit Care Med, 199: 321–332. February 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{oelsner_albuminuria_2019,\n\ttitle = {Albuminuria, {Lung} {Function} {Decline}, and {Risk} of {Incident} {Chronic} {Obstructive} {Pulmonary} {Disease}. {The} {NHLBI} {Pooled} {Cohorts} {Study}.},\n\tvolume = {199},\n\tissn = {1535-4970},\n\tdoi = {10.1164/rccm.201803-0402OC},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{RATIONALE: }Chronic lower respiratory diseases (CLRDs), including chronic obstructive pulmonary disease (COPD) and asthma, are the fourth leading cause of death. Prior studies suggest that albuminuria, a biomarker of endothelial injury, is increased in patients with COPD.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{OBJECTIVES: }To test whether albuminuria was associated with lung function decline and incident CLRDs.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{METHODS: }Six U.S. population-based cohorts were harmonized and pooled. Participants with prevalent clinical lung disease were excluded. Albuminuria (urine albumin-to-creatinine ratio) was measured in spot samples. Lung function was assessed by spirometry. Incident CLRD-related hospitalizations and deaths were classified via adjudication and/or administrative criteria. Mixed and proportional hazards models were used to test individual-level associations adjusted for age, height, weight, sex, race/ethnicity, education, birth year, cohort, smoking status, pack-years of smoking, renal function, hypertension, diabetes, and medications.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{MEASUREMENTS AND MAIN RESULTS: }Among 10,961 participants with preserved lung function, mean age at albuminuria measurement was 60 years, 51\\% were never-smokers, median albuminuria was 5.6 mg/g, and mean FEV decline was 31.5 ml/yr. For each SD increase in log-transformed albuminuria, there was 2.81\\% greater FEV decline (95\\% confidence interval [CI], 0.86-4.76\\%; P = 0.0047), 11.02\\% greater FEV/FVC decline (95\\% CI, 4.43-17.62\\%; P = 0.0011), and 15\\% increased hazard of incident spirometry-defined moderate-to-severe COPD (95\\% CI, 2-31\\%, P = 0.0021). Each SD log-transformed albuminuria increased hazards of incident COPD-related hospitalization/mortality by 26\\% (95\\% CI, 18-34\\%, P {\\textless} 0.0001) among 14,213 participants followed for events. Asthma events were not significantly associated. Associations persisted in participants without current smoking, diabetes, hypertension, or cardiovascular disease.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSIONS: }Albuminuria was associated with greater lung function decline, incident spirometry-defined COPD, and incident COPD-related events in a U.S. population-based sample.{\\textless}/p{\\textgreater}},\n\tjournal = {Am J Respir Crit Care Med},\n\tauthor = {Oelsner, Elizabeth C and Balte, Pallavi P and Grams, Morgan E and Cassano, Patricia A and Jacobs, David R and Barr, R Graham and Burkart, Kristin M and Kalhan, Ravi and Kronmal, Richard and Loehr, Laura R and O’Connor, George T and Schwartz, Joseph E and Shlipak, Michael and Tracy, Russell P and Tsai, Michael Y and White, Wendy and Yende, Sachin},\n\tmonth = feb,\n\tyear = {2019},\n\tpages = {321--332},\n}\n\n\n\n

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\n \\textlessp\\textgreater\\textbfRATIONALE: Chronic lower respiratory diseases (CLRDs), including chronic obstructive pulmonary disease (COPD) and asthma, are the fourth leading cause of death. Prior studies suggest that albuminuria, a biomarker of endothelial injury, is increased in patients with COPD.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfOBJECTIVES: To test whether albuminuria was associated with lung function decline and incident CLRDs.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfMETHODS: Six U.S. population-based cohorts were harmonized and pooled. Participants with prevalent clinical lung disease were excluded. Albuminuria (urine albumin-to-creatinine ratio) was measured in spot samples. Lung function was assessed by spirometry. Incident CLRD-related hospitalizations and deaths were classified via adjudication and/or administrative criteria. Mixed and proportional hazards models were used to test individual-level associations adjusted for age, height, weight, sex, race/ethnicity, education, birth year, cohort, smoking status, pack-years of smoking, renal function, hypertension, diabetes, and medications.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfMEASUREMENTS AND MAIN RESULTS: Among 10,961 participants with preserved lung function, mean age at albuminuria measurement was 60 years, 51% were never-smokers, median albuminuria was 5.6 mg/g, and mean FEV decline was 31.5 ml/yr. For each SD increase in log-transformed albuminuria, there was 2.81% greater FEV decline (95% confidence interval [CI], 0.86-4.76%; P = 0.0047), 11.02% greater FEV/FVC decline (95% CI, 4.43-17.62%; P = 0.0011), and 15% increased hazard of incident spirometry-defined moderate-to-severe COPD (95% CI, 2-31%, P = 0.0021). Each SD log-transformed albuminuria increased hazards of incident COPD-related hospitalization/mortality by 26% (95% CI, 18-34%, P \\textless 0.0001) among 14,213 participants followed for events. Asthma events were not significantly associated. Associations persisted in participants without current smoking, diabetes, hypertension, or cardiovascular disease.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfCONCLUSIONS: Albuminuria was associated with greater lung function decline, incident spirometry-defined COPD, and incident COPD-related events in a U.S. population-based sample.\\textless/p\\textgreater\n

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\n \n\n \n \n Garg, P. K; Biggs, M. L; Barzilay, J.; Djoussé, L.; Hirsch, C.; Ix, J. H; Kizer, J. R; Tracy, R. P; Newman, A. B; Siscovick, D. S; and Mukamal, K. J\n\n\n \n \n \n \n Advanced glycation end product carboxymethyl-lysine and risk of incident peripheral artery disease in older adults: The Cardiovascular Health Study.\n \n \n \n\n\n \n\n\n\n Diab Vasc Dis Res,1479164119847481. May 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{garg_advanced_2019,\n\ttitle = {Advanced glycation end product carboxymethyl-lysine and risk of incident peripheral artery disease in older adults: {The} {Cardiovascular} {Health} {Study}.},\n\tissn = {1752-8984},\n\tdoi = {10.1177/1479164119847481},\n\tabstract = {{\\textless}p{\\textgreater}Carboxymethyl-lysine is an advanced glycation end product that is detectable in the serum. Higher carboxymethyl-lysine levels have been associated with increased risk of coronary heart disease, stroke and cardiovascular mortality. We determined whether high carboxymethyl-lysine levels are also associated with the risk of peripheral artery disease in Cardiovascular Health Study participants who were all aged 65 years and older at baseline. Multivariate Cox proportional hazards models were used to determine the association of baseline carboxymethyl-lysine levels with incident peripheral artery disease in 3267 individuals followed for a median length of 10.0 years. A total of 157 cases of incident peripheral artery disease occurred during follow-up. No significant relationship between carboxymethyl-lysine and risk of peripheral artery disease was found (hazard ratio per standard deviation increment = 1.03; 95\\% confidence interval = 0.87, 1.23).{\\textless}/p{\\textgreater}},\n\tjournal = {Diab Vasc Dis Res},\n\tauthor = {Garg, Parveen K and Biggs, Mary L and Barzilay, Joshua and Djoussé, Luc and Hirsch, Calvin and Ix, Joachim H and Kizer, Jorge R and Tracy, Russell P and Newman, Anne B and Siscovick, David S and Mukamal, Kenneth J},\n\tmonth = may,\n\tyear = {2019},\n\tpages = {1479164119847481},\n}\n\n\n\n

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\n \n\n \n \n Wang, H.; Cade, B. E; Sofer, T.; Sands, S. A; Chen, H.; Browning, S. R; Stilp, A. M; Louie, T. L; Thornton, T. A; Johnson, W C.; Below, J. E; Conomos, M. P; Evans, D. S; Gharib, S. A; Guo, X.; Wood, A. C; Mei, H.; Yaffe, K.; Loredo, J. S; Ramos, A. R; Barrett-Connor, E.; Ancoli-Israel, S.; Zee, P. C; Arens, R.; Shah, N. A; Taylor, K. D; Tranah, G. J; Stone, K. L; Hanis, C. L; Wilson, J. G; Gottlieb, D. J; Patel, S. R; Rice, K.; Post, W. S; Rotter, J. I; Sunyaev, S. R; Cai, J.; Lin, X.; Purcell, S. M; Laurie, C. C; Saxena, R.; Redline, S.; and Zhu, X.\n\n\n \n \n \n \n Admixture mapping identifies novel loci for obstructive sleep apnea in Hispanic/Latino Americans.\n \n \n \n\n\n \n\n\n\n Hum Mol Genet, 28: 675–687. 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{wang_admixture_2019,\n\ttitle = {Admixture mapping identifies novel loci for obstructive sleep apnea in {Hispanic}/{Latino} {Americans}.},\n\tvolume = {28},\n\tissn = {1460-2083},\n\tdoi = {10.1093/hmg/ddy387},\n\tabstract = {{\\textless}p{\\textgreater}Obstructive sleep apnea (OSA) is a common disorder associated with increased risk of cardiovascular disease and mortality. Its prevalence and severity vary across ancestral background. Although OSA traits are heritable, few genetic associations have been identified. To identify genetic regions associated with OSA and improve statistical power, we applied admixture mapping on three primary OSA traits [the apnea hypopnea index (AHI), overnight average oxyhemoglobin saturation (SaO2) and percentage time SaO2 {\\textless} 90\\%] and a secondary trait (respiratory event duration) in a Hispanic/Latino American population study of 11 575 individuals with significant variation in ancestral background. Linear mixed models were performed using previously inferred African, European and Amerindian local genetic ancestry markers. Global African ancestry was associated with a lower AHI, higher SaO2 and shorter event duration. Admixture mapping analysis of the primary OSA traits identified local African ancestry at the chromosomal region 2q37 as genome-wide significantly associated with AHI (P {\\textless} 5.7 × 10-5), and European and Amerindian ancestries at 18q21 suggestively associated with both AHI and percentage time SaO2 {\\textless} 90\\% (P {\\textless} 10-3). Follow-up joint ancestry-SNP association analyses identified novel variants in ferrochelatase (FECH), significantly associated with AHI and percentage time SaO2 {\\textless} 90\\% after adjusting for multiple tests (P {\\textless} 8 × 10-6). These signals contributed to the admixture mapping associations and were replicated in independent cohorts. In this first admixture mapping study of OSA, novel associations with variants in the iron/heme metabolism pathway suggest a role for iron in influencing respiratory traits underlying OSA.{\\textless}/p{\\textgreater}},\n\tjournal = {Hum Mol Genet},\n\tauthor = {Wang, Heming and Cade, Brian E and Sofer, Tamar and Sands, Scott A and Chen, Han and Browning, Sharon R and Stilp, Adrienne M and Louie, Tin L and Thornton, Timothy A and Johnson, W Craig and Below, Jennifer E and Conomos, Matthew P and Evans, Daniel S and Gharib, Sina A and Guo, Xiuqing and Wood, Alexis C and Mei, Hao and Yaffe, Kristine and Loredo, Jose S and Ramos, Alberto R and Barrett-Connor, Elizabeth and Ancoli-Israel, Sonia and Zee, Phyllis C and Arens, Raanan and Shah, Neomi A and Taylor, Kent D and Tranah, Gregory J and Stone, Katie L and Hanis, Craig L and Wilson, James G and Gottlieb, Daniel J and Patel, Sanjay R and Rice, Ken and Post, Wendy S and Rotter, Jerome I and Sunyaev, Shamil R and Cai, Jianwen and Lin, Xihong and Purcell, Shaun M and Laurie, Cathy C and Saxena, Richa and Redline, Susan and Zhu, Xiaofeng},\n\tyear = {2019},\n\tpages = {675--687},\n}\n\n\n\n

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\n \n\n \n \n Nanna, M. G; Peterson, E. D; Wojdyla, D.; and Navar, A. M.\n\n\n \n \n \n \n The Accuracy of Cardiovascular Pooled Cohort Risk Estimates in U.S. Older Adults.\n \n \n \n\n\n \n\n\n\n J Gen Intern Med. October 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{nanna_accuracy_2019,\n\ttitle = {The {Accuracy} of {Cardiovascular} {Pooled} {Cohort} {Risk} {Estimates} in {U}.{S}. {Older} {Adults}.},\n\tissn = {1525-1497},\n\tdoi = {10.1007/s11606-019-05361-4},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{BACKGROUND: }The ACC/AHA guidelines for primary prevention rely on the Pooled Cohort Risk Equations (PCE) risk estimates of atherosclerotic cardiovascular disease (ASCVD) to guide treatment decisions. In light of the PCE being derived in younger populations, their accuracy in older adults is uncertain.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{OBJECTIVE: }To evaluate the predictive accuracy and calibration of the PCE in older individuals.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{DESIGN AND SETTING: }We estimated CVD predicted and observed risk among individuals from four large prospective cohort studies: Cardiovascular Health Study, Multiethnic Study of Atherosclerosis, Framingham Original, and Framingham Offspring.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{PARTICIPANTS: }12,527 overall individuals without ASCVD, including 9864 individuals aged 40-74 years and 2663 aged {\\textgreater}=75 years.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{MEASUREMENTS: }We examined the operating characteristics of the PCE to estimate 5-year risk of stroke, MI, and CHD death overall and by age and sex strata. The associations between individual components of the PCE and cardiovascular events by age group ({\\textgreater}=75 vs 40-74 years) were also evaluated.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{RESULTS: }The PCE had low discrimination for 5-year ASCVD risk in older ({\\textgreater}=75 years) (c-statistic = 0.62, 95\\% CI 0.60-0.65) vs. younger (40-74 years) adults (c-statistic = 0.75, 95\\% CI 0.73-0.76). Calibration of the PCE was suboptimal in both older and younger adults, overestimating risk in the highest risk groups. Performance of the PCE in older adults was similarly poor when stratified by sex and age {\\textgreater}= 80 years.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{LIMITATIONS: }Since the PCE were derived from similar cohorts, though using different age groups and exams, this analysis likely overestimates the performance of the PCE.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSION: }The performance of the PCE for ASCVD risk estimation in older adults is suboptimal; new models to effectively risk-stratify older adults are needed.{\\textless}/p{\\textgreater}},\n\tjournal = {J Gen Intern Med},\n\tauthor = {Nanna, Michael G and Peterson, Eric D and Wojdyla, Daniel and Navar, Ann Marie},\n\tmonth = oct,\n\tyear = {2019},\n}\n\n\n\n

\n\n\n

\n \\textlessp\\textgreater\\textbfBACKGROUND: The ACC/AHA guidelines for primary prevention rely on the Pooled Cohort Risk Equations (PCE) risk estimates of atherosclerotic cardiovascular disease (ASCVD) to guide treatment decisions. In light of the PCE being derived in younger populations, their accuracy in older adults is uncertain.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfOBJECTIVE: To evaluate the predictive accuracy and calibration of the PCE in older individuals.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfDESIGN AND SETTING: We estimated CVD predicted and observed risk among individuals from four large prospective cohort studies: Cardiovascular Health Study, Multiethnic Study of Atherosclerosis, Framingham Original, and Framingham Offspring.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfPARTICIPANTS: 12,527 overall individuals without ASCVD, including 9864 individuals aged 40-74 years and 2663 aged \\textgreater=75 years.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfMEASUREMENTS: We examined the operating characteristics of the PCE to estimate 5-year risk of stroke, MI, and CHD death overall and by age and sex strata. The associations between individual components of the PCE and cardiovascular events by age group (\\textgreater=75 vs 40-74 years) were also evaluated.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfRESULTS: The PCE had low discrimination for 5-year ASCVD risk in older (\\textgreater=75 years) (c-statistic = 0.62, 95% CI 0.60-0.65) vs. younger (40-74 years) adults (c-statistic = 0.75, 95% CI 0.73-0.76). Calibration of the PCE was suboptimal in both older and younger adults, overestimating risk in the highest risk groups. Performance of the PCE in older adults was similarly poor when stratified by sex and age \\textgreater= 80 years.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfLIMITATIONS: Since the PCE were derived from similar cohorts, though using different age groups and exams, this analysis likely overestimates the performance of the PCE.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfCONCLUSION: The performance of the PCE for ASCVD risk estimation in older adults is suboptimal; new models to effectively risk-stratify older adults are needed.\\textless/p\\textgreater\n

\n\n\n

\n \n\n \n \n Ellervik, C.; Roselli, C.; Christophersen, I. E; Alonso, A.; Pietzner, M.; Sitlani, C. M; Trompet, S.; Arking, D. E; Geelhoed, B.; Guo, X.; Kleber, M. E; Lin, H. J; Lin, H.; Macfarlane, P.; Selvin, E.; Shaffer, C.; Smith, A. V; Verweij, N.; Weiss, S.; Cappola, A. R; Dörr, M.; Gudnason, V.; Heckbert, S.; Mooijaart, S.; März, W.; Psaty, B. M; Ridker, P. M; Roden, D.; Stott, D. J; Völzke, H.; Benjamin, E. J; Delgado, G.; Ellinor, P.; Homuth, G.; Köttgen, A.; Jukema, J. W; Lubitz, S. A; Mora, S.; Rienstra, M.; Rotter, J. I; Shoemaker, M B.; Sotoodehnia, N.; Taylor, K. D; van der Harst, P.; Albert, C. M; and Chasman, D. I\n\n\n \n \n \n \n Assessment of the Relationship Between Genetic Determinants of Thyroid Function and Atrial Fibrillation: A Mendelian Randomization Study.\n \n \n \n\n\n \n\n\n\n JAMA Cardiol. January 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{ellervik_assessment_2019,\n\ttitle = {Assessment of the {Relationship} {Between} {Genetic} {Determinants} of {Thyroid} {Function} and {Atrial} {Fibrillation}: {A} {Mendelian} {Randomization} {Study}.},\n\tissn = {2380-6591},\n\tdoi = {10.1001/jamacardio.2018.4635},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{Importance: }Increased free thyroxine (FT4) and decreased thyrotropin are associated with increased risk of atrial fibrillation (AF) in observational studies, but direct involvement is unclear.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{Objective: }To evaluate the potential direct involvement of thyroid traits on AF.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{Design, Setting, and Participants: }Study-level mendelian randomization (MR) included 11 studies, and summary-level MR included 55 114 AF cases and 482 295 referents, all of European ancestry.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{Exposures: }Genomewide significant variants were used as instruments for standardized FT4 and thyrotropin levels within the reference range, standardized triiodothyronine (FT3):FT4 ratio, hypothyroidism, standardized thyroid peroxidase antibody levels, and hyperthyroidism. Mendelian randomization used genetic risk scores in study-level analysis or individual single-nucleotide polymorphisms in 2-sample MR for the summary-level data.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{Main Outcomes and Measures: }Prevalent and incident AF.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{Results: }The study-level analysis included 7679 individuals with AF and 49 233 referents (mean age [standard error], 62 [3] years; 15 859 men [29.7\\%]). In study-level random-effects meta-analysis, the pooled hazard ratio of FT4 levels (nanograms per deciliter) for incident AF was 1.55 (95\\% CI, 1.09-2.20; P = .02; I2 = 76\\%) and the pooled odds ratio (OR) for prevalent AF was 2.80 (95\\% CI, 1.41-5.54; P = .003; I2 = 64\\%) in multivariable-adjusted analyses. The FT4 genetic risk score was associated with an increase in FT4 by 0.082 SD (standard error, 0.007; P {\\textless} .001) but not with incident AF (risk ratio, 0.84; 95\\% CI, 0.62-1.14; P = .27) or prevalent AF (OR, 1.32; 95\\% CI, 0.64-2.73; P = .46). Similarly, in summary-level inverse-variance weighted random-effects MR, gene-based FT4 within the reference range was not associated with AF (OR, 1.01; 95\\% CI, 0.89-1.14; P = .88). However, gene-based increased FT3:FT4 ratio, increased thyrotropin within the reference range, and hypothyroidism were associated with AF with inverse-variance weighted random-effects OR of 1.33 (95\\% CI, 1.08-1.63; P = .006), 0.88 (95\\% CI, 0.84-0.92; P {\\textless} .001), and 0.94 (95\\% CI, 0.90-0.99; P = .009), respectively, and robust to tests of horizontal pleiotropy. However, the subset of hypothyroidism single-nucleotide polymorphisms involved in autoimmunity and thyroid peroxidase antibodies levels were not associated with AF. Gene-based hyperthyroidism was associated with AF with MR-Egger OR of 1.31 (95\\% CI, 1.05-1.63; P = .02) with evidence of horizontal pleiotropy (P = .045).{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{Conclusions and Relevance: }Genetically increased FT3:FT4 ratio and hyperthyroidism, but not FT4 within the reference range, were associated with increased AF, and increased thyrotropin within the reference range and hypothyroidism were associated with decreased AF, supporting a pathway involving the pituitary-thyroid-cardiac axis.{\\textless}/p{\\textgreater}},\n\tjournal = {JAMA Cardiol},\n\tauthor = {Ellervik, Christina and Roselli, Carolina and Christophersen, Ingrid E and Alonso, Alvaro and Pietzner, Maik and Sitlani, Collen M and Trompet, Stella and Arking, Dan E and Geelhoed, Bastiaan and Guo, Xiuqing and Kleber, Marcus E and Lin, Henry J and Lin, Honghuang and Macfarlane, Peter and Selvin, Elizabeth and Shaffer, Christian and Smith, Albert V and Verweij, Niek and Weiss, Stefan and Cappola, Anne R and Dörr, Marcus and Gudnason, Vilmundur and Heckbert, Susan and Mooijaart, Simon and März, Winfried and Psaty, Bruce M and Ridker, Paul M and Roden, Dan and Stott, David J and Völzke, Henry and Benjamin, Emelia J and Delgado, Graciela and Ellinor, Patrick and Homuth, Georg and Köttgen, Anna and Jukema, Johan W and Lubitz, Steven A and Mora, Samia and Rienstra, Michiel and Rotter, Jerome I and Shoemaker, M Benjamin and Sotoodehnia, Nona and Taylor, Kent D and van der Harst, Pim and Albert, Christine M and Chasman, Daniel I},\n\tmonth = jan,\n\tyear = {2019},\n}\n\n\n\n

\n\n\n

\n \\textlessp\\textgreater\\textbfImportance: Increased free thyroxine (FT4) and decreased thyrotropin are associated with increased risk of atrial fibrillation (AF) in observational studies, but direct involvement is unclear.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfObjective: To evaluate the potential direct involvement of thyroid traits on AF.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfDesign, Setting, and Participants: Study-level mendelian randomization (MR) included 11 studies, and summary-level MR included 55 114 AF cases and 482 295 referents, all of European ancestry.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfExposures: Genomewide significant variants were used as instruments for standardized FT4 and thyrotropin levels within the reference range, standardized triiodothyronine (FT3):FT4 ratio, hypothyroidism, standardized thyroid peroxidase antibody levels, and hyperthyroidism. Mendelian randomization used genetic risk scores in study-level analysis or individual single-nucleotide polymorphisms in 2-sample MR for the summary-level data.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfMain Outcomes and Measures: Prevalent and incident AF.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfResults: The study-level analysis included 7679 individuals with AF and 49 233 referents (mean age [standard error], 62 [3] years; 15 859 men [29.7%]). In study-level random-effects meta-analysis, the pooled hazard ratio of FT4 levels (nanograms per deciliter) for incident AF was 1.55 (95% CI, 1.09-2.20; P = .02; I2 = 76%) and the pooled odds ratio (OR) for prevalent AF was 2.80 (95% CI, 1.41-5.54; P = .003; I2 = 64%) in multivariable-adjusted analyses. The FT4 genetic risk score was associated with an increase in FT4 by 0.082 SD (standard error, 0.007; P \\textless .001) but not with incident AF (risk ratio, 0.84; 95% CI, 0.62-1.14; P = .27) or prevalent AF (OR, 1.32; 95% CI, 0.64-2.73; P = .46). Similarly, in summary-level inverse-variance weighted random-effects MR, gene-based FT4 within the reference range was not associated with AF (OR, 1.01; 95% CI, 0.89-1.14; P = .88). However, gene-based increased FT3:FT4 ratio, increased thyrotropin within the reference range, and hypothyroidism were associated with AF with inverse-variance weighted random-effects OR of 1.33 (95% CI, 1.08-1.63; P = .006), 0.88 (95% CI, 0.84-0.92; P \\textless .001), and 0.94 (95% CI, 0.90-0.99; P = .009), respectively, and robust to tests of horizontal pleiotropy. However, the subset of hypothyroidism single-nucleotide polymorphisms involved in autoimmunity and thyroid peroxidase antibodies levels were not associated with AF. Gene-based hyperthyroidism was associated with AF with MR-Egger OR of 1.31 (95% CI, 1.05-1.63; P = .02) with evidence of horizontal pleiotropy (P = .045).\\textless/p\\textgreater\\textlessp\\textgreater\\textbfConclusions and Relevance: Genetically increased FT3:FT4 ratio and hyperthyroidism, but not FT4 within the reference range, were associated with increased AF, and increased thyrotropin within the reference range and hypothyroidism were associated with decreased AF, supporting a pathway involving the pituitary-thyroid-cardiac axis.\\textless/p\\textgreater\n

\n\n\n

\n \n\n \n \n Dixit, S.; Whooley, M. A; Vittinghoff, E.; Roberts, J. D; Heckbert, S. R; Fitzpatrick, A. L; Lin, J.; Leung, C.; Mukamal, K. J; and Marcus, G. M\n\n\n \n \n \n \n Alcohol consumption and leukocyte telomere length.\n \n \n \n\n\n \n\n\n\n Sci Rep, 9: 1404. February 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{dixit_alcohol_2019,\n\ttitle = {Alcohol consumption and leukocyte telomere length.},\n\tvolume = {9},\n\tissn = {2045-2322},\n\tdoi = {10.1038/s41598-019-38904-0},\n\tabstract = {{\\textless}p{\\textgreater}The relationship between alcohol consumption and mortality generally exhibits a U-shaped curve. The longevity observed with moderate alcohol consumption may be explained by other confounding factors, and, if such a relationship is present, the mechanism is not well understood. Indeed, the optimal amount of alcohol consumption for health has yet to be determined. Leukocyte telomere length is an emerging quantifiable marker of biological age and health, and a shorter telomere length is a predictor of increased mortality. Because leukocyte telomere length is a quantifiable and objectively measurable biomarker of aging, we sought to identify the amount of alcohol consumption associated with the longest telomere length and least telomere length attrition. Among over 2,000 participants from two distinct cohort studies, we found no pattern of alcohol consumption that was associated with longer telomere length or less telomere length attrition over time. Binge drinking may reduce telomere length. Using telomere length as a marker of age and health, these data fail to demonstrate any benefits of alcohol consumption, even when consumed in moderation.{\\textless}/p{\\textgreater}},\n\tjournal = {Sci Rep},\n\tauthor = {Dixit, Shalini and Whooley, Mary A and Vittinghoff, Eric and Roberts, Jason D and Heckbert, Susan R and Fitzpatrick, Annette L and Lin, Jue and Leung, Cindy and Mukamal, Kenneth J and Marcus, Gregory M},\n\tmonth = feb,\n\tyear = {2019},\n\tpages = {1404},\n}\n\n\n\n

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\n \n\n \n \n Stacey, R. B.; Zgibor, J.; Leaverton, P. E; Schocken, D. D; Peregoy, J. A; Lyles, M. F; Bertoni, A. G; and Burke, G. L\n\n\n \n \n \n \n Abnormal Fasting Glucose Increases Risk of Unrecognized Myocardial Infarctions in an Elderly Cohort.\n \n \n \n\n\n \n\n\n\n J Am Geriatr Soc, 67: 43–49. January 2019.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{stacey_abnormal_2019,\n\ttitle = {Abnormal {Fasting} {Glucose} {Increases} {Risk} of {Unrecognized} {Myocardial} {Infarctions} in an {Elderly} {Cohort}.},\n\tvolume = {67},\n\tissn = {1532-5415},\n\tdoi = {10.1111/jgs.15604},\n\tabstract = {{\\textless}p{\\textgreater}\\textbf{OBJECTIVES: }To investigate glucose levels as a risk factor for unrecognized myocardial infarctions (UMIs).{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{DESIGN: }Cohort SETTING: Cardiovascular Health Study.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{PARTICIPANTS: }Individuals aged 65 and older with fasting glucose measurements (N=4,355; normal fasting glucose (NFG), n = 2,041; impaired fasting glucose (IFG), n = 1,706; DM: n = 608; 40\\% male, 84\\% white, mean age 72.4 ± 5.6).{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{MEASUREMENTS: }The relationship between glucose levels and UMI was examined. Participants with prior coronary heart disease (CHD) or UMI on initial electrocardiography were excluded. Using Minnesota codes, UMI was identified according to the presence of pathological Q-waves or minor Q-waves with ST-T abnormalities. Crude and adjusted hazard ratios (HRs) were calculated. Analyses were adjusted for age, sex, body mass index (BMI), hypertension, antihypertensive and lipid-lowering medication use, total cholesterol, high-density lipoprotein cholesterol, and smoking status.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{RESULTS: }Over a mean follow-up of 6 years, there were 459 incident UMIs (NFG, n=202; IFG, n=183; DM, n=74). Participants with IFG were slightly more likely than those with NFG to experience a UMI (hazard ratio (HR)=1.11, 95\\% confidence interval (CI)=0.91-1.36, p = .30), and those with DM were more likely than those with NFG to experience a UMI (HR=1.65, 95\\% CI=1.25-2.13, p {\\textless} .001). After adjustment HR for UMI in IFG those with IFG were no more likely than those with NFG to experience a UMI (HR=1.01, 95\\% CI=0.82-1.24, p = .93), whereas those with DM were more likely than those with NFG to experience a UMI (HR=1.37, 95\\% CI=1.02-1.81, p = .03). The 2-hour oral glucose tolerance test was not statistically significantly associated with UMI.{\\textless}/p{\\textgreater}{\\textless}p{\\textgreater}\\textbf{CONCLUSION: }Fasting glucose status, particularly in the diabetic range, forecasted UMI during 6 years of follow-up in elderly adults. Further studies are needed to clarify the level of glucose at which risk is greater. J Am Geriatr Soc 67:43-49, 2019.{\\textless}/p{\\textgreater}},\n\tjournal = {J Am Geriatr Soc},\n\tauthor = {Stacey, Richard Brandon and Zgibor, Janice and Leaverton, Paul E and Schocken, Douglas D and Peregoy, Jennifer A and Lyles, Mary F and Bertoni, Alain G and Burke, Gregory L},\n\tmonth = jan,\n\tyear = {2019},\n\tpages = {43--49},\n}\n\n\n\n\n\n\n\n\n\n\n\n

\n\n\n

\n \\textlessp\\textgreater\\textbfOBJECTIVES: To investigate glucose levels as a risk factor for unrecognized myocardial infarctions (UMIs).\\textless/p\\textgreater\\textlessp\\textgreater\\textbfDESIGN: Cohort SETTING: Cardiovascular Health Study.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfPARTICIPANTS: Individuals aged 65 and older with fasting glucose measurements (N=4,355; normal fasting glucose (NFG), n = 2,041; impaired fasting glucose (IFG), n = 1,706; DM: n = 608; 40% male, 84% white, mean age 72.4 ± 5.6).\\textless/p\\textgreater\\textlessp\\textgreater\\textbfMEASUREMENTS: The relationship between glucose levels and UMI was examined. Participants with prior coronary heart disease (CHD) or UMI on initial electrocardiography were excluded. Using Minnesota codes, UMI was identified according to the presence of pathological Q-waves or minor Q-waves with ST-T abnormalities. Crude and adjusted hazard ratios (HRs) were calculated. Analyses were adjusted for age, sex, body mass index (BMI), hypertension, antihypertensive and lipid-lowering medication use, total cholesterol, high-density lipoprotein cholesterol, and smoking status.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfRESULTS: Over a mean follow-up of 6 years, there were 459 incident UMIs (NFG, n=202; IFG, n=183; DM, n=74). Participants with IFG were slightly more likely than those with NFG to experience a UMI (hazard ratio (HR)=1.11, 95% confidence interval (CI)=0.91-1.36, p = .30), and those with DM were more likely than those with NFG to experience a UMI (HR=1.65, 95% CI=1.25-2.13, p \\textless .001). After adjustment HR for UMI in IFG those with IFG were no more likely than those with NFG to experience a UMI (HR=1.01, 95% CI=0.82-1.24, p = .93), whereas those with DM were more likely than those with NFG to experience a UMI (HR=1.37, 95% CI=1.02-1.81, p = .03). The 2-hour oral glucose tolerance test was not statistically significantly associated with UMI.\\textless/p\\textgreater\\textlessp\\textgreater\\textbfCONCLUSION: Fasting glucose status, particularly in the diabetic range, forecasted UMI during 6 years of follow-up in elderly adults. Further studies are needed to clarify the level of glucose at which risk is greater. J Am Geriatr Soc 67:43-49, 2019.\\textless/p\\textgreater\n

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\n \n\n \n \n Kuo, I.; Liu, T.; Patrick, R.; Trezza, C.; Bazerman, L.; Uhrig Castonguay, B. J.; Peterson, J.; Kurth, A.; and Beckwith, C. G.\n\n\n \n \n \n \n \n Use of an mHealth Intervention to Improve Engagement in HIV Community-Based Care Among Persons Recently Released from a Correctional Facility in Washington, DC: A Pilot Study.\n \n \n \n \n\n\n \n\n\n\n AIDS and Behavior. January 2019.\n \n\n\n\n
\n\n\n\n \n \n $\"Use$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{kuo_use_2019,\n\ttitle = {Use of an {mHealth} {Intervention} to {Improve} {Engagement} in {HIV} {Community}-{Based} {Care} {Among} {Persons} {Recently} {Released} from a {Correctional} {Facility} in {Washington}, {DC}: {A} {Pilot} {Study}},\n\tissn = {1573-3254},\n\tshorttitle = {Use of an {mHealth} {Intervention} to {Improve} {Engagement} in {HIV} {Community}-{Based} {Care} {Among} {Persons} {Recently} {Released} from a {Correctional} {Facility} in {Washington}, {DC}},\n\turl = {https://doi.org/10.1007/s10461-018-02389-1},\n\tdoi = {10.1007/s10461-018-02389-1},\n\tabstract = {We examined the preliminary effectiveness of a computerized counseling session plus post-incarceration text messaging intervention (CARE + Corrections) to support ART adherence and linkage/engagement in community care among recently incarcerated persons with HIV in Washington, D.C. Recently incarcerated persons with HIV ≥ 18 years old were recruited from the D.C. jail or community outreach and randomized to CARE + Corrections or control arm. Participants completed assessments at baseline, 3-months and 6-months. Multivariable random effects modeling identified predictors of suppressed viral load (≤ 200 copies/mL) and engagement in HIV care at 6 months. Participants (N = 110) were aged 42 (IQR 30–49); 58\\% male, 24\\% female, 18\\% transgender, 85\\% Black, and lifetime incarceration was a median of 7 years (IQR 2–15). More controls had a regular healthcare provider at baseline. Although not statistically significant, intervention participants had increased odds of viral suppression versus controls at 6 months (AOR 2.04; 95\\% CI 0.62, 6.70). Those reporting high ART adherence at baseline had higher odds of viral suppression at follow-up (AOR 10.77; 95\\% CI 1.83, 63.31). HIV care engagement was similar between the two groups, although both groups reported increased engagement at 6 months versus baseline. We observed a positive but non-significant association of viral suppression in the CARE + Corrections group, and care engagement increased in both groups after 6 months. Further attention to increasing viral suppression among CJ-involved persons with HIV upon community reentry is warranted.},\n\tlanguage = {en},\n\turldate = {2019-01-19},\n\tjournal = {AIDS and Behavior},\n\tauthor = {Kuo, Irene and Liu, Tao and Patrick, Rudy and Trezza, Claudia and Bazerman, Lauri and Uhrig Castonguay, Breana J. and Peterson, James and Kurth, Ann and Beckwith, Curt G.},\n\tmonth = jan,\n\tyear = {2019},\n\tkeywords = {Engagement in care, HIV, Incarcerated persons, mHealth},\n}\n\n\n\n

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\n \n 2018\n \n \n (14)\n \n \n

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\n \n\n \n \n McCollister et. al.\n\n\n \n \n \n \n \n Criminal justice measures for economic data harmonization in substance use disorder research.\n \n \n \n \n\n\n \n\n\n\n September 2018.\n \n\n\n\n
\n\n\n\n \n \n $\"Criminal$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n\n\n\n

@misc{mccollister_et_al_criminal_2018,\n\ttitle = {Criminal justice measures for economic data harmonization in substance use disorder research},\n\turl = {https://healthandjusticejournal.biomedcentral.com/articles/10.1186/s40352-018-0073-6},\n\turldate = {2018-12-03},\n\tauthor = {{McCollister et. al.}},\n\tmonth = sep,\n\tyear = {2018},\n\tkeywords = {STTR Core},\n}\n\n\n\n

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\n \n\n \n \n Stevens, E. R; Nucifora, K.; Zhou, Q.; Braithwaite, R. S.; Cleland, C. M.; Ritchie, A. S.; Kutnick, A. H.; and Gwadz, M. V\n\n\n \n \n \n \n \n Cost-effectiveness of peer- versus venue-based approaches for detecting undiagnosed HIV among heterosexuals in high-risk New York City neighborhoods.\n \n \n \n \n\n\n \n\n\n\n Journal of acquired immune deficiency syndromes (1999), 77(2): 183–192. February 2018.\n \n\n\n\n
\n\n\n\n \n \n $\"Cost-effectiveness$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{stevens_cost-effectiveness_2018,\n\ttitle = {Cost-effectiveness of peer- versus venue-based approaches for detecting undiagnosed {HIV} among heterosexuals in high-risk {New} {York} {City} neighborhoods},\n\tvolume = {77},\n\tissn = {1525-4135},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5762425/},\n\tdoi = {10.1097/QAI.0000000000001578},\n\tabstract = {Introduction\nWe used a computer simulation of HIV progression and transmission to evaluate the cost-effectiveness of a scale-up of three strategies to seek out and test individuals with undiagnosed HIV in New York City (NYC).\n\nSetting\nHypothetical NYC population\n\nMethods\nWe incorporated the observed effects and costs of the three “seek and test” strategies in a computer simulation of HIV in NYC, comparing a scenario in which the strategies were scaled up with a one-year implementation or a long-term implementation with a counterfactual scenario with no scale-up. The simulation combined a deterministic compartmental model of HIV transmission with a stochastic microsimulation of HIV progression, calibrated to NYC epidemiological data from 2003 to 2015. The three approaches were respondent driven sampling (RDS) with anonymous HIV testing (“RDS-A”), RDS with a two-session confidential HIV testing approach (“RDS-C”), and venue-based sampling (“VBS”).\n\nResults\nRDS-A was the most cost-effective strategy tested. When implemented for only one year and then stopped thereafter, using a societal perspective, the cost per quality-adjusted life-year (QALY) gained versus no intervention was \\$812/QALY, \\$18,110/QALY, and \\$20,362/QALY for RDS-A, RDS-C, and VBS, respectively. When interventions were implemented long-term, the cost per QALY gained versus no intervention was cost-saving, \\$31,773/QALY, and \\$35,148/QALY for RDS-A, RDS-C, and VBS, respectively. When compared to RDS-A the incremental cost effectiveness ratios (ICERs) for both VBS and RDS-C were dominated.\n\nConclusion\nThe expansion of the RDS-A strategy would substantially reduce HIV-related deaths and new HIV infections in NYC, and would be either cost-saving or have favorable cost-effectiveness.},\n\tnumber = {2},\n\turldate = {2019-02-26},\n\tjournal = {Journal of acquired immune deficiency syndromes (1999)},\n\tauthor = {Stevens, Elizabeth R and Nucifora, Kimberly and Zhou, Qinlian and Braithwaite, R. Scott and Cleland, Charles M. and Ritchie, Amanda S. and Kutnick, Alexandra H. and Gwadz, Marya V},\n\tmonth = feb,\n\tyear = {2018},\n\tpmid = {29135654},\n\tpmcid = {PMC5762425},\n\tpages = {183--192},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Gordon, M. S.; Crable, E. L.; Carswell, S. B.; Leopold, J.; Hodo-Powell, J.; McKenzie, M.; and Rich, J. D.\n\n\n \n \n \n \n \n A Randomized Controlled Trial of Intensive Case Management (Project Bridge) for HIV-Infected Probationers and Parolees.\n \n \n \n \n\n\n \n\n\n\n AIDS and Behavior, 22(3): 1030–1038. March 2018.\n \n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{gordon_randomized_2018,\n\ttitle = {A {Randomized} {Controlled} {Trial} of {Intensive} {Case} {Management} ({Project} {Bridge}) for {HIV}-{Infected} {Probationers} and {Parolees}},\n\tvolume = {22},\n\tissn = {1573-3254},\n\turl = {https://doi.org/10.1007/s10461-017-2016-y},\n\tdoi = {10.1007/s10461-017-2016-y},\n\tabstract = {Individuals on probation and parole are disproportionately at high risk for HIV infection and experience significant barriers to accessing health care. This study was a two-group randomized controlled trial conducted at a community corrections office and was designed to link HIV positive probationers/parolees to HIV treatment in the community. HIV positive participants were assigned to one of the two treatment conditions: (1) Project Bridge (PB), an intensive case-management intervention; or (2) treatment as usual (TAU), involving standard referral to treatment. We hypothesized that PB would be more effective than TAU in terms of initiating individuals in community HIV treatment. We found no difference in rates of, or time to, treatment initiation when comparing the PB to TAU (all ns {\\textgreater} 0.05). Additionally, there was no statistically significant difference between HIV medication regiment initiation by treatment condition (p {\\textgreater} 0.05). Despite limitations, we found that probationers and parolees were willing to be screened and linked to treatment.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2018-12-03},\n\tjournal = {AIDS and Behavior},\n\tauthor = {Gordon, Michael S. and Crable, Erika L. and Carswell, Steven B. and Leopold, Jessica and Hodo-Powell, Jennifer and McKenzie, Michelle and Rich, Josiah D.},\n\tmonth = mar,\n\tyear = {2018},\n\tkeywords = {Case management, Community HIV treatment, Libertad condicional, Manejo de casos, Parole, Período de prueba, Probation, Tratamientos de VIH comunitario},\n\tpages = {1030--1038},\n}\n\n\n\n\n\n\n\n

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\n \n\n \n \n Hussong, et al.\n\n\n \n \n \n \n \n Approaches for creating comparable measures of alcohol use symptoms: Harmonization with eight studies of criminal justice populations - ScienceDirect.\n \n \n \n \n\n\n \n\n\n\n October 2018.\n \n\n\n\n
\n\n\n\n \n \n $\"Approaches$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n\n\n\n

@misc{hussong_et_al._approaches_2018,\n\ttitle = {Approaches for creating comparable measures of alcohol use symptoms: {Harmonization} with eight studies of criminal justice populations - {ScienceDirect}},\n\turl = {https://www.sciencedirect.com/science/article/pii/S0376871618305076?via%3Dihub},\n\turldate = {2018-12-03},\n\tauthor = {{Hussong, et al.}},\n\tmonth = oct,\n\tyear = {2018},\n\tkeywords = {STTR Core},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Delaney, J. A.; Nance, R. M.; Whitney, B. M.; Altice, F. L.; Dong, X.; Trejo, M. E. P.; Matsuzaki, M.; Taxman, F. S.; Chander, G.; Kuo, I.; Fredericksen, R.; Strand, L. N.; Eron, J. J.; Geng, E.; Kitahata, M. M.; Mathews, W. C.; Mayer, K.; Moore, R. D.; Saag, M. S.; Springer, S.; Chandler, R.; Kahana, S.; and Crane, H. M.\n\n\n \n \n \n \n \n Brief Report: Reduced Use of Illicit Substances, Even Without Abstinence, Is Associated With Improved Depressive Symptoms Among People Living With Hiv.\n \n \n \n \n\n\n \n\n\n\n Jaids Journal of Acquired Immune Deficiency Syndromes, 79(3): 283–287. November 2018.\n \n\n\n\n
\n\n\n\n \n \n $\"Brief$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n\n\n\n

@article{delaney_brief_2018,\n\ttitle = {Brief {Report}: {Reduced} {Use} of {Illicit} {Substances}, {Even} {Without} {Abstinence}, {Is} {Associated} {With} {Improved} {Depressive} {Symptoms} {Among} {People} {Living} {With} {Hiv}},\n\tvolume = {79},\n\tissn = {1525-4135},\n\tshorttitle = {Brief {Report}},\n\turl = {https://insights.ovid.com/pubmed?pmid=30036277},\n\tdoi = {10.1097/QAI.0000000000001803},\n\tabstract = {\\textbf{Purpose:}{\\textless}p{\\textgreater}Substance use is linked with poor outcomes among people living with HIV (PLWH) and is associated with mental health disorders. This analysis examines the impact of decreasing substance use, even without abstinence, on depressive symptoms among PLWH.{\\textless}/p{\\textgreater}\\textbf{Methods:}{\\textless}p{\\textgreater}Data are from PLWH enrolled in the Centers for AIDS Research Network of Integrated Clinical Sites cohort. Participants completed longitudinal assessments of substance use (modified ASSIST) and depressive symptoms (PHQ-9). Changes in substance use frequency were categorized as abstinence, reduced use, and nondecreasing use. Adjusted linear mixed models with time-updated change in substance use frequency and depressive symptom scores were used to examine associations between changes in the use of individual substances and depressive symptoms. Analyses were repeated using joint longitudinal survival models to examine associations with a high (PHQ-9 ≥10) score.{\\textless}/p{\\textgreater}\\textbf{Results:}{\\textless}p{\\textgreater}Among 9905 PLWH, 728 used cocaine/crack, 1016 used amphetamine-type substances (ATS), 290 used illicit opiates, and 3277 used marijuana at baseline. Changes in ATS use were associated with the greatest improvements in depressive symptoms: stopping ATS led to a mean decrease of PHQ-9 by 2.2 points (95\\% CI: 1.8 to 2.7) and a 61\\% lower odds of PHQ-9 score ≥10 (95\\% CI: 0.30 to 0.52), and decreasing ATS use led to a mean decrease of 1.7 points (95\\% CI: 1.2 to 2.3) and a 62\\% lower odds of PHQ-9 score ≥10 (95\\% CI: 0.25 to 0.56). Stopping and reducing marijuana and stopping cocaine/crack use were also associated with improvement in depressive symptoms.{\\textless}/p{\\textgreater}\\textbf{Conclusions:}{\\textless}p{\\textgreater}We demonstrated that both substance use reduction and abstinence are associated with improvements in depressive symptoms over time.{\\textless}/p{\\textgreater}},\n\tlanguage = {ENGLISH},\n\tnumber = {3},\n\turldate = {2018-12-03},\n\tjournal = {Jaids Journal of Acquired Immune Deficiency Syndromes},\n\tauthor = {Delaney, Joseph A. and Nance, Robin M. and Whitney, Bridget M. and Altice, Frederick L. and Dong, Xinyuan and Trejo, Maria Esther Perez and Matsuzaki, Mika and Taxman, Faye S. and Chander, Geetanjali and Kuo, Irene and Fredericksen, Rob and Strand, Lauren N. and Eron, Joseph J. and Geng, Elvin and Kitahata, Mari M. and Mathews, William C. and Mayer, Kenneth and Moore, Richard D. and Saag, Michael S. and Springer, Sandra and Chandler, Redonna and Kahana, Shoshana and Crane, Heidi M.},\n\tmonth = nov,\n\tyear = {2018},\n\tpmid = {00126334-201811010-00001},\n\tkeywords = {STTR Core},\n\tpages = {283--287},\n}\n\n\n\n

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\n \n\n \n \n Gwadz, M.; Leonard, N. R.; Honig, S.; Freeman, R.; Kutnick, A.; and Ritchie, A. S.\n\n\n \n \n \n \n \n Doing battle with “the monster:” how high-risk heterosexuals experience and successfully manage HIV stigma as a barrier to HIV testing.\n \n \n \n \n\n\n \n\n\n\n International Journal for Equity in Health, 17. April 2018.\n \n\n\n\n
\n\n\n\n \n \n $\"Doing$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{gwadz_doing_2018,\n\ttitle = {Doing battle with “the monster:” how high-risk heterosexuals experience and successfully manage {HIV} stigma as a barrier to {HIV} testing},\n\tvolume = {17},\n\tissn = {1475-9276},\n\tshorttitle = {Doing battle with “the monster},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5910579/},\n\tdoi = {10.1186/s12939-018-0761-9},\n\tabstract = {Background\nAnnual HIV testing is recommended for populations at-risk for HIV in the United States, including heterosexuals geographically connected to urban high-risk areas (HRA) with elevated rates of HIV prevalence and poverty, who are primarily African American/Black or Hispanic. Yet this subpopulation of “individuals residing in HRA” (IR-HRA) evidence low rates of regular HIV testing. HIV stigma is a recognized primary barrier to testing, in part due to its interaction with other stigmatized social identities. Guided by social-cognitive and intersectionality theories, this qualitative descriptive study explored stigma as a barrier to HIV testing and identified ways IR-HRA manage stigma.\n\nMethods\nIn 2012-2014, we conducted in-depth qualitative interviews with 31 adult IR-HRA (74\\% male, 84\\% African American/Black) with unknown or negative HIV status, purposively sampled from a larger study for maximum variation on HIV testing experiences. Interviews were audio-recorded and professionally transcribed verbatim. Data were analyzed using a systematic content analysis approach that was both theory-driven and inductive.\n\nResults\nStigma was a primary barrier to HIV testing among IR-HRA. In the context of an under-resourced community, HIV stigma was experienced as emerging from, and being perpetuated by, health care organizations and educational institutions, as well as community members. Participants noted it was “better not to know” one’s HIV status, to avoid experiencing HIV-related stigma, which could interact with other stigmatized social identities and threaten vital social relationships, life chances, and resources. Yet most had tested for HIV previously. Factors facilitating testing included health education to boost knowledge of effective treatments for HIV; understanding HIV does not necessitate ending social relationships; and tapping into altruism.\n\nConclusions\nIn the context of economic and social inequality, HIV stigma operates on multiple, intersecting layers. IR-HRA struggle with an aversion to HIV testing, because adopting another stigmatized status is dangerous. They also find ways to manage stigma to engage in testing, even if not at recommended levels. Findings highlight strategies to reduce HIV stigma at the levels of communities, institutions, and individuals to improve rates of annual HIV testing necessary to eliminate HIV transmission and reduce HIV-related racial and ethnic health disparities among IR-HRA.},\n\turldate = {2018-11-20},\n\tjournal = {International Journal for Equity in Health},\n\tauthor = {Gwadz, Marya and Leonard, Noelle R. and Honig, Sylvie and Freeman, Robert and Kutnick, Alexandra and Ritchie, Amanda S.},\n\tmonth = apr,\n\tyear = {2018},\n\tpmid = {29678188},\n\tpmcid = {PMC5910579},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n Background Annual HIV testing is recommended for populations at-risk for HIV in the United States, including heterosexuals geographically connected to urban high-risk areas (HRA) with elevated rates of HIV prevalence and poverty, who are primarily African American/Black or Hispanic. Yet this subpopulation of “individuals residing in HRA” (IR-HRA) evidence low rates of regular HIV testing. HIV stigma is a recognized primary barrier to testing, in part due to its interaction with other stigmatized social identities. Guided by social-cognitive and intersectionality theories, this qualitative descriptive study explored stigma as a barrier to HIV testing and identified ways IR-HRA manage stigma. Methods In 2012-2014, we conducted in-depth qualitative interviews with 31 adult IR-HRA (74% male, 84% African American/Black) with unknown or negative HIV status, purposively sampled from a larger study for maximum variation on HIV testing experiences. Interviews were audio-recorded and professionally transcribed verbatim. Data were analyzed using a systematic content analysis approach that was both theory-driven and inductive. Results Stigma was a primary barrier to HIV testing among IR-HRA. In the context of an under-resourced community, HIV stigma was experienced as emerging from, and being perpetuated by, health care organizations and educational institutions, as well as community members. Participants noted it was “better not to know” one’s HIV status, to avoid experiencing HIV-related stigma, which could interact with other stigmatized social identities and threaten vital social relationships, life chances, and resources. Yet most had tested for HIV previously. Factors facilitating testing included health education to boost knowledge of effective treatments for HIV; understanding HIV does not necessitate ending social relationships; and tapping into altruism. Conclusions In the context of economic and social inequality, HIV stigma operates on multiple, intersecting layers. IR-HRA struggle with an aversion to HIV testing, because adopting another stigmatized status is dangerous. They also find ways to manage stigma to engage in testing, even if not at recommended levels. Findings highlight strategies to reduce HIV stigma at the levels of communities, institutions, and individuals to improve rates of annual HIV testing necessary to eliminate HIV transmission and reduce HIV-related racial and ethnic health disparities among IR-HRA.\n

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\n \n\n \n \n Spaulding, A. C.; Drobeniuc, A.; Frew, P. M.; Lemon, T. L.; Anderson, E. J.; Cerwonka, C.; Bowden, C.; Freshley, J.; and del Rio, C.\n\n\n \n \n \n \n \n Jail, an unappreciated medical home: Assessing the feasibility of a strengths-based case management intervention to improve the care retention of HIV-infected persons once released from jail.\n \n \n \n \n\n\n \n\n\n\n PLoS ONE, 13(3). March 2018.\n \n\n\n\n
\n\n\n\n \n \n $\"Jail,$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{spaulding_jail_2018,\n\ttitle = {Jail, an unappreciated medical home: {Assessing} the feasibility of a strengths-based case management intervention to improve the care retention of {HIV}-infected persons once released from jail},\n\tvolume = {13},\n\tissn = {1932-6203},\n\tshorttitle = {Jail, an unappreciated medical home},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5877830/},\n\tdoi = {10.1371/journal.pone.0191643},\n\tabstract = {Background\nLinkage to and retention in care for US persons living with HIV (PLWH) after release from jail usually declines. We know of no rigorously evaluated behavioral interventions that can improve this. We hypothesized that a strengths-based case management intervention that we developed for PLWH leaving jail would increase linkage/retention in care (indicated by receipt of laboratory draws) and a suppressed HIV viral load (VL) in the year following release.\n\nMethods and findings\nWe conducted a quasi-experimental feasibility study of our intervention for PLWH jailed in Atlanta. We recruited 113 PLWH in jail starting in 2014. “SUCCESS” (Sustained, Unbroken Connection to Care, Entry Services, and Suppression) began in jail and continued post-release. Subjects who started the intervention but subsequently began long-term incarcerations were excluded from further analysis. Persons who were retained in the intervention group were compared to contemporaneously incarcerated PLWH who did not receive the intervention. Identities were submitted to an enhanced HIV/AIDS reporting system (eHARS) at the state health department to capture all laboratories drawn. Both community engagement and care upon jail return were assessed equally. For 44 intervention participants released to Atlanta, 50\\% of care occurred on subsequent jail stays, as documented with EventFlow software. Forty-five receiving usual services only were recruited for comparison. By examining records of jail reentries, half of participants and 60\\% of controls recidivated (range: 1–8 returns). All but 6 participants in the intervention and 9 subjects in the comparison arm had ≥1 laboratory recorded in eHARS post-release. Among the intervention group, 52\\% were retained in care (i.e., had two laboratory studies, {\\textgreater} = 3 months apart), versus 40\\% among the comparison group (OR = 1.60, 95\\% CI (0.71, 3.81)). Both arms showed improved viral load suppression.\n\nConclusions\nThere was a trend towards increased retention for PLWH released from jail after SUCCESS, compared to usual services. Measuring linkage at all venues, including jail-based clinics, fully captured engagement for this frequently recidivating population.\n\nTrial registration\nClinicalTrials.gov NCT02185742},\n\tnumber = {3},\n\turldate = {2018-06-22},\n\tjournal = {PLoS ONE},\n\tauthor = {Spaulding, Anne C. and Drobeniuc, Ana and Frew, Paula M. and Lemon, Tiffany L. and Anderson, Emeli J. and Cerwonka, Colin and Bowden, Chava and Freshley, John and del Rio, Carlos},\n\tmonth = mar,\n\tyear = {2018},\n\tpmid = {29601591},\n\tpmcid = {PMC5877830},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n Background Linkage to and retention in care for US persons living with HIV (PLWH) after release from jail usually declines. We know of no rigorously evaluated behavioral interventions that can improve this. We hypothesized that a strengths-based case management intervention that we developed for PLWH leaving jail would increase linkage/retention in care (indicated by receipt of laboratory draws) and a suppressed HIV viral load (VL) in the year following release. Methods and findings We conducted a quasi-experimental feasibility study of our intervention for PLWH jailed in Atlanta. We recruited 113 PLWH in jail starting in 2014. “SUCCESS” (Sustained, Unbroken Connection to Care, Entry Services, and Suppression) began in jail and continued post-release. Subjects who started the intervention but subsequently began long-term incarcerations were excluded from further analysis. Persons who were retained in the intervention group were compared to contemporaneously incarcerated PLWH who did not receive the intervention. Identities were submitted to an enhanced HIV/AIDS reporting system (eHARS) at the state health department to capture all laboratories drawn. Both community engagement and care upon jail return were assessed equally. For 44 intervention participants released to Atlanta, 50% of care occurred on subsequent jail stays, as documented with EventFlow software. Forty-five receiving usual services only were recruited for comparison. By examining records of jail reentries, half of participants and 60% of controls recidivated (range: 1–8 returns). All but 6 participants in the intervention and 9 subjects in the comparison arm had ≥1 laboratory recorded in eHARS post-release. Among the intervention group, 52% were retained in care (i.e., had two laboratory studies, \\textgreater = 3 months apart), versus 40% among the comparison group (OR = 1.60, 95% CI (0.71, 3.81)). Both arms showed improved viral load suppression. Conclusions There was a trend towards increased retention for PLWH released from jail after SUCCESS, compared to usual services. Measuring linkage at all venues, including jail-based clinics, fully captured engagement for this frequently recidivating population. Trial registration ClinicalTrials.gov NCT02185742\n

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\n \n\n \n \n Smith, M. K.; Solomon, S. S.; Cummings, D. A. T.; Srikrishnan, A. K.; Kumar, M. S.; Vasudevan, C. K.; McFall, A. M.; Lucas, G. M.; Celentano, D. D.; and Mehta, S. H.\n\n\n \n \n \n \n \n Overlap between harm reduction and HIV service utilisation among PWID in India: Implications for HIV combination prevention.\n \n \n \n \n\n\n \n\n\n\n International Journal of Drug Policy, 57: 111–118. July 2018.\n \n\n\n\n
\n\n\n\n \n \n $\"Overlap$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{smith_overlap_2018,\n\ttitle = {Overlap between harm reduction and {HIV} service utilisation among {PWID} in {India}: {Implications} for {HIV} combination prevention},\n\tvolume = {57},\n\tissn = {0955-3959},\n\tshorttitle = {Overlap between harm reduction and {HIV} service utilisation among {PWID} in {India}},\n\turl = {http://www.sciencedirect.com/science/article/pii/S0955395918300422},\n\tdoi = {10.1016/j.drugpo.2018.02.007},\n\tabstract = {Background\nIn some regions, HIV incidence is rising among people who inject drugs (PWID). Combination prevention approaches are well suited to PWID who face multiple sources of HIV risk. This analysis investigates patterns of utilisation to basic HIV services (HIV counselling and testing [HCT], antiretroviral therapy [ART]) as well as harm reduction programs (needle and syringe exchange programs [NSEP] and opioid agonist therapy [OAT]) among PWID and how utilisation of harm reduction services is associated with HIV-related care seeking behaviours.\nMethods\nRespondent-driven sampling was used to recruit 14,481 PWID across 15 cities in India. Sampling-weighted multilevel logistic regression models assessed associations between utilisation of harm reduction service and HCT and ART use among those indicated (90.3\\% and 5.0\\% of full sample, respectively). We considered both recent (prior year) and ever use of services.\nResults\nOverall, 42.3\\% reported prior HIV testing and 57.9\\% of eligible persons reported ART initiation, but overlap with NSEP and OAT use was limited. In adjusted models, recent and ever use of both NSEP and OAT were significantly associated with recent and ever HCT utilisation, respectively; however, harm reduction utilisation was not associated with ART initiation among eligible participants.\nConclusions\nHarm reduction services may play a key role in linking PWID with HIV testing; however, they were not associated with ART initiation among eligible individuals. Moreover, a large majority who utilised NSEP and OAT were not engaged in optimal HIV care or prevention, highlighting missed opportunities and a need for stronger linkages between NSEP/OAT and HIV care and treatment, particularly among those actively injecting. These findings provide key insights to better understand how services can be linked or combined to optimise service utilisation among PWID.},\n\turldate = {2018-06-22},\n\tjournal = {International Journal of Drug Policy},\n\tauthor = {Smith, M. Kumi and Solomon, Sunil S. and Cummings, Derek A. T. and Srikrishnan, Aylur K. and Kumar, M. Suresh and Vasudevan, C. K. and McFall, Allison M. and Lucas, Gregory M. and Celentano, David D. and Mehta, Shruti H.},\n\tmonth = jul,\n\tyear = {2018},\n\tkeywords = {HIV, Harm reduction, India, Injection drug use},\n\tpages = {111--118},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Beckwith, C. G.; Kuo, I.; Fredericksen, R. J.; Brinkley-Rubinstein, L.; Cunningham, W. E.; Springer, S. A.; Loeliger, K. B.; Franks, J.; Christopoulos, K.; Lorvick, J.; Kahana, S. Y.; Young, R.; Seal, D. W.; Zawitz, C.; Delaney, J. A.; Crane, H. M.; and Biggs, M. L.\n\n\n \n \n \n \n \n Risk behaviors and HIV care continuum outcomes among criminal justice-involved HIV-infected transgender women and cisgender men: Data from the Seek, Test, Treat, and Retain Harmonization Initiative.\n \n \n \n \n\n\n \n\n\n\n PLoS ONE, 13(5). May 2018.\n \n\n\n\n
\n\n\n\n \n \n $\"Risk$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n\n\n\n

@article{beckwith_risk_2018,\n\ttitle = {Risk behaviors and {HIV} care continuum outcomes among criminal justice-involved {HIV}-infected transgender women and cisgender men: {Data} from the {Seek}, {Test}, {Treat}, and {Retain} {Harmonization} {Initiative}},\n\tvolume = {13},\n\tissn = {1932-6203},\n\tshorttitle = {Risk behaviors and {HIV} care continuum outcomes among criminal justice-involved {HIV}-infected transgender women and cisgender men},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5963777/},\n\tdoi = {10.1371/journal.pone.0197730},\n\tabstract = {Background\nTransgender persons are highly victimized, marginalized, disproportionately experience incarceration, and have alarmingly increased rates of HIV infection compared to cis-gender persons. Few studies have examined the HIV care continuum outcomes among transgender women (TW), particularly TW who are involved with the criminal justice (CJ) system.\n\nMethods\nTo improve our understanding of HIV care continuum outcomes and risk behaviors among HIV-infected TW who are involved with the CJ system, we analyzed data from the National Institute on Drug Abuse-supported Seek, Test, Treat, Retain (STTR) Data Harmonization Initiative. Baseline data were pooled and analyzed from three U.S. STTR studies to examine HIV risk and care continuum indicators among CJ-involved HIV-infected TW compared to cisgender men (CM), matched on age (within 5 years) and study at a ratio of 1:5.\n\nResults\nEighty-eight TW and 440 CM were included in the study. Among matched participants, TW were more likely to report crack and cocaine use compared to CM (40\\%,16\\% respectively, p{\\textless}0.001); both TW and CM reported high rates of condomless sex (58\\%, 64\\%, respectively); TW were more likely than CM to have more than one sexual partner (OR = 2.9, 95\\% CI: 1.6, 5.2; p{\\textless}0.001) and have engaged in exchange sex (OR = 3.9, 95\\% CI: 2.3, 6.6; p{\\textless}0.001). There were no significant differences between TW and CM in the percentage currently taking ART (52\\%, 49\\%, respectively), the mean percent adherence to ART (77\\% for both groups), and the proportion who achieved viral suppression (61\\%, 58\\%, respectively).\n\nConclusions\nHIV-infected CJ-involved TW and CM had similar use of ART and viral suppression but TW were more likely than matched CM to engage in exchange sex, have multiple sexual partners, and use crack/cocaine. TW and CM had similarly high rates of condomless sex and use of other drugs. TW require tailored risk reduction interventions, however both CJ-involved TW and CM require focused attention to reduce HIV risk and improve HIV continuum of care outcomes.},\n\tnumber = {5},\n\turldate = {2018-06-21},\n\tjournal = {PLoS ONE},\n\tauthor = {Beckwith, Curt G. and Kuo, Irene and Fredericksen, Rob J. and Brinkley-Rubinstein, Lauren and Cunningham, William E. and Springer, Sandra A. and Loeliger, Kelsey B. and Franks, Julie and Christopoulos, Katerina and Lorvick, Jennifer and Kahana, Shoshana Y. and Young, Rebekah and Seal, David W. and Zawitz, Chad and Delaney, Joseph A. and Crane, Heidi M. and Biggs, Mary L.},\n\tmonth = may,\n\tyear = {2018},\n\tpmid = {29787580},\n\tpmcid = {PMC5963777},\n\tkeywords = {STTR Core},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n Background Transgender persons are highly victimized, marginalized, disproportionately experience incarceration, and have alarmingly increased rates of HIV infection compared to cis-gender persons. Few studies have examined the HIV care continuum outcomes among transgender women (TW), particularly TW who are involved with the criminal justice (CJ) system. Methods To improve our understanding of HIV care continuum outcomes and risk behaviors among HIV-infected TW who are involved with the CJ system, we analyzed data from the National Institute on Drug Abuse-supported Seek, Test, Treat, Retain (STTR) Data Harmonization Initiative. Baseline data were pooled and analyzed from three U.S. STTR studies to examine HIV risk and care continuum indicators among CJ-involved HIV-infected TW compared to cisgender men (CM), matched on age (within 5 years) and study at a ratio of 1:5. Results Eighty-eight TW and 440 CM were included in the study. Among matched participants, TW were more likely to report crack and cocaine use compared to CM (40%,16% respectively, p\\textless0.001); both TW and CM reported high rates of condomless sex (58%, 64%, respectively); TW were more likely than CM to have more than one sexual partner (OR = 2.9, 95% CI: 1.6, 5.2; p\\textless0.001) and have engaged in exchange sex (OR = 3.9, 95% CI: 2.3, 6.6; p\\textless0.001). There were no significant differences between TW and CM in the percentage currently taking ART (52%, 49%, respectively), the mean percent adherence to ART (77% for both groups), and the proportion who achieved viral suppression (61%, 58%, respectively). Conclusions HIV-infected CJ-involved TW and CM had similar use of ART and viral suppression but TW were more likely than matched CM to engage in exchange sex, have multiple sexual partners, and use crack/cocaine. TW and CM had similarly high rates of condomless sex and use of other drugs. TW require tailored risk reduction interventions, however both CJ-involved TW and CM require focused attention to reduce HIV risk and improve HIV continuum of care outcomes.\n

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\n \n\n \n \n Matsuzaki, M.; Vu, Q. M.; Gwadz, M.; Delaney, J. A. C.; Kuo, I.; Trejo, M. E. P.; Cunningham, W. E.; Cunningham, C. O.; and Christopoulos, K.\n\n\n \n \n \n \n \n Perceived access and barriers to care among illicit drug users and hazardous drinkers: findings from the Seek, Test, Treat, and Retain data harmonization initiative (STTR).\n \n \n \n \n\n\n \n\n\n\n BMC Public Health, 18. March 2018.\n \n\n\n\n
\n\n\n\n \n \n $\"Perceived$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n\n\n\n

@article{matsuzaki_perceived_2018,\n\ttitle = {Perceived access and barriers to care among illicit drug users and hazardous drinkers: findings from the {Seek}, {Test}, {Treat}, and {Retain} data harmonization initiative ({STTR})},\n\tvolume = {18},\n\tissn = {1471-2458},\n\tshorttitle = {Perceived access and barriers to care among illicit drug users and hazardous drinkers},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5859651/},\n\tdoi = {10.1186/s12889-018-5291-2},\n\tabstract = {Background\nIllicit drug use (DU) and hazardous drinking (HD) among marginalized populations may be associated with greater barriers to care.\n\nMethods\nWe used baseline data on the participants of the Seek, Test, Treat, and Retain data harmonization initiative. DU includes use of any illicit drugs within the past 6 months. HD was defined as scores ≥8 for men and ≥ 7 for women on Alcohol Use Disorders Identification Test within the past 12 months. Social support scores were assigned by summing scores from individual questions related to social support. Two outcomes for multivariable regression models and mediation analysis were perceived access to care and perceived barriers to care scores, calculated from summated points from individual questions within each domain. All models were adjusted for age, gender, race/ethnicity, and social support and stratified by HIV status.\n\nResults\nAmong 1403 illicit drug users and 4984 non-drug users, the mean age was 39.6 ± 12.2 years old, 71\\% were male, 57\\% African Americans, and 39\\% Hispanic/Latinos. Over 25\\% reported difficulties in covering medical costs and finding transportation to health care facilities and greater proportions of drug users and hazardous drinkers reported these issues than non-DU/non-HD. In multivariable models, DU and HD were both independently associated with having greater barriers to care (β: 0.49 (95\\% confidence interval: 0.19 to 0.79) p {\\textless} 0.01; 0.31 (0.18 to 0.45) {\\textless} 0.01) in HIV-negative participants. Neither DU nor HD was strongly associated with barriers to care for HIV-positive participants. Social support was associated with better perceived access to care and fewer barriers to care in the HIV-negative participants.\n\nConclusion\nThe current study found that financial burdens of care, logistical difficulties in accessing care, and low social support were common challenges among individuals using illicit drugs and/or drinking hazardously. Addressing structural barriers and strengthening social support may be important strategies to improve health care among marginalized populations, regardless of HIV status.\n\nElectronic supplementary material\nThe online version of this article (10.1186/s12889-018-5291-2) contains supplementary material, which is available to authorized users.},\n\turldate = {2018-06-21},\n\tjournal = {BMC Public Health},\n\tauthor = {Matsuzaki, Mika and Vu, Quan M. and Gwadz, Marya and Delaney, Joseph A. C. and Kuo, Irene and Trejo, Maria Esther Perez and Cunningham, William E. and Cunningham, Chinazo O. and Christopoulos, Katerina},\n\tmonth = mar,\n\tyear = {2018},\n\tpmid = {29554894},\n\tpmcid = {PMC5859651},\n\tkeywords = {STTR Core},\n}\n\n\n\n\n\n\n\n

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\n Background Illicit drug use (DU) and hazardous drinking (HD) among marginalized populations may be associated with greater barriers to care. Methods We used baseline data on the participants of the Seek, Test, Treat, and Retain data harmonization initiative. DU includes use of any illicit drugs within the past 6 months. HD was defined as scores ≥8 for men and ≥ 7 for women on Alcohol Use Disorders Identification Test within the past 12 months. Social support scores were assigned by summing scores from individual questions related to social support. Two outcomes for multivariable regression models and mediation analysis were perceived access to care and perceived barriers to care scores, calculated from summated points from individual questions within each domain. All models were adjusted for age, gender, race/ethnicity, and social support and stratified by HIV status. Results Among 1403 illicit drug users and 4984 non-drug users, the mean age was 39.6 ± 12.2 years old, 71% were male, 57% African Americans, and 39% Hispanic/Latinos. Over 25% reported difficulties in covering medical costs and finding transportation to health care facilities and greater proportions of drug users and hazardous drinkers reported these issues than non-DU/non-HD. In multivariable models, DU and HD were both independently associated with having greater barriers to care (β: 0.49 (95% confidence interval: 0.19 to 0.79) p \\textless 0.01; 0.31 (0.18 to 0.45) \\textless 0.01) in HIV-negative participants. Neither DU nor HD was strongly associated with barriers to care for HIV-positive participants. Social support was associated with better perceived access to care and fewer barriers to care in the HIV-negative participants. Conclusion The current study found that financial burdens of care, logistical difficulties in accessing care, and low social support were common challenges among individuals using illicit drugs and/or drinking hazardously. Addressing structural barriers and strengthening social support may be important strategies to improve health care among marginalized populations, regardless of HIV status. Electronic supplementary material The online version of this article (10.1186/s12889-018-5291-2) contains supplementary material, which is available to authorized users.\n

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\n \n\n \n \n Cunningham, W. E.; Weiss, R. E.; Nakazono, T.; Malek, M. A.; Shoptaw, S. J.; Ettner, S. L.; and Harawa, N. T.\n\n\n \n \n \n \n \n Effectiveness of a Peer Navigation Intervention to Sustain Viral Suppression Among HIV-Positive Men and Transgender Women Released From Jail: The LINK LA Randomized Clinical Trial.\n \n \n \n \n\n\n \n\n\n\n JAMA Internal Medicine, 178(4): 542–553. April 2018.\n \n\n\n\n
\n\n\n\n \n \n $\"Effectiveness$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{cunningham_effectiveness_2018,\n\ttitle = {Effectiveness of a {Peer} {Navigation} {Intervention} to {Sustain} {Viral} {Suppression} {Among} {HIV}-{Positive} {Men} and {Transgender} {Women} {Released} {From} {Jail}: {The} {LINK} {LA} {Randomized} {Clinical} {Trial}},\n\tvolume = {178},\n\tissn = {2168-6106},\n\tshorttitle = {Effectiveness of a {Peer} {Navigation} {Intervention} to {Sustain} {Viral} {Suppression} {Among} {HIV}-{Positive} {Men} and {Transgender} {Women} {Released} {From} {Jail}},\n\turl = {https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2673736},\n\tdoi = {10.1001/jamainternmed.2018.0150},\n\tabstract = {{\\textless}h3{\\textgreater}Importance{\\textless}/h3{\\textgreater}{\\textless}p{\\textgreater}Diagnosis of human immunodeficiency virus (HIV) infection, linkage and retention in care, and adherence to antiretroviral therapy are steps in the care continuum enabling consistent viral suppression for people living with HIV, extending longevity and preventing further transmission. While incarcerated, people living with HIV receive antiretroviral therapy and achieve viral suppression more consistently than after they are released. No interventions have shown sustained viral suppression after jail release.{\\textless}/p{\\textgreater}{\\textless}h3{\\textgreater}Objective{\\textless}/h3{\\textgreater}{\\textless}p{\\textgreater}To test the effect on viral suppression in released inmates of the manualized LINK LA (Linking Inmates to Care in Los Angeles) peer navigation intervention compared with standard transitional case management controls.{\\textless}/p{\\textgreater}{\\textless}h3{\\textgreater}Design, Setting, and Participants{\\textless}/h3{\\textgreater}{\\textless}p{\\textgreater}Randomized clinical trial conducted from December 2012 through October 2016 with people living with HIV being released from Los Angeles (LA) County Jail. All participants were (1) 18 years or older; (2) either men or transgender women diagnosed with HIV; (3) English speaking; (4) selected for the transitional case management program prior to enrollment; (5) residing in LA County; and (6) eligible for antiretroviral therapy.{\\textless}/p{\\textgreater}{\\textless}h3{\\textgreater}Main Outcomes and Measures{\\textless}/h3{\\textgreater}{\\textless}p{\\textgreater}Change in HIV viral suppression (\\&lt;75 copies/mL) over a 12-month period.{\\textless}/p{\\textgreater}{\\textless}h3{\\textgreater}Interventions{\\textless}/h3{\\textgreater}{\\textless}p{\\textgreater}During the 12-session, 24-week LINK LA Peer Navigation intervention, trained peer navigators counseled participants on goal setting and problem solving around barriers to HIV care and adherence, starting while the participants were still in jail. After their release, they continued counseling while they accompanied participants to 2 HIV care visits, then facilitated communication with clinicians during visits.{\\textless}/p{\\textgreater}{\\textless}h3{\\textgreater}Results{\\textless}/h3{\\textgreater}{\\textless}p{\\textgreater}Of 356 participants randomized, 151 (42\\%) were black; 110 (31\\%) were Latino; 303 (85\\%) were men; 53 (15\\%) were transgender women; and the mean (SD) age was 39.5 (10.4) years. At 12 months, viral suppression was achieved by 62 (49.6\\%) of 125 participants in the peer navigation (intervention) arm compared with 45 (36.0\\%) of 125 in the transitional case management (control) arm, for an unadjusted treatment difference of 13.6\\% (95\\% CI, 1.34\\%-25.9\\%;\\textit{P} = .03). In the repeated measures, random effects, logistic model the adjusted probability of viral suppression declined from 52\\% at baseline to 30\\% among controls, while those in the peer navigation arm maintained viral suppression at 49\\% from baseline to 12 months, for a difference-in-difference of 22\\% (95\\% CI, 0.03-0.41;\\textit{P} = .02).{\\textless}/p{\\textgreater}{\\textless}h3{\\textgreater}Conclusions and Relevance{\\textless}/h3{\\textgreater}{\\textless}p{\\textgreater}The LINK LA peer navigation intervention was successful at preventing declines in viral suppression, typically seen after release from incarceration, compared with standard transitional case management. Future research should examine ways to strengthen the intervention to increase viral suppression above baseline levels.{\\textless}/p{\\textgreater}{\\textless}h3{\\textgreater}Trial Registration{\\textless}/h3{\\textgreater}{\\textless}p{\\textgreater}clinicaltrials.gov Identifier:NCT01406626{\\textless}/p{\\textgreater}},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2018-04-25},\n\tjournal = {JAMA Internal Medicine},\n\tauthor = {Cunningham, William E. and Weiss, Robert E. and Nakazono, Terry and Malek, Mark A. and Shoptaw, Steve J. and Ettner, Susan L. and Harawa, Nina T.},\n\tmonth = apr,\n\tyear = {2018},\n\tpages = {542--553},\n}\n\n\n\n

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\n \\textlessh3\\textgreaterImportance\\textless/h3\\textgreater\\textlessp\\textgreaterDiagnosis of human immunodeficiency virus (HIV) infection, linkage and retention in care, and adherence to antiretroviral therapy are steps in the care continuum enabling consistent viral suppression for people living with HIV, extending longevity and preventing further transmission. While incarcerated, people living with HIV receive antiretroviral therapy and achieve viral suppression more consistently than after they are released. No interventions have shown sustained viral suppression after jail release.\\textless/p\\textgreater\\textlessh3\\textgreaterObjective\\textless/h3\\textgreater\\textlessp\\textgreaterTo test the effect on viral suppression in released inmates of the manualized LINK LA (Linking Inmates to Care in Los Angeles) peer navigation intervention compared with standard transitional case management controls.\\textless/p\\textgreater\\textlessh3\\textgreaterDesign, Setting, and Participants\\textless/h3\\textgreater\\textlessp\\textgreaterRandomized clinical trial conducted from December 2012 through October 2016 with people living with HIV being released from Los Angeles (LA) County Jail. All participants were (1) 18 years or older; (2) either men or transgender women diagnosed with HIV; (3) English speaking; (4) selected for the transitional case management program prior to enrollment; (5) residing in LA County; and (6) eligible for antiretroviral therapy.\\textless/p\\textgreater\\textlessh3\\textgreaterMain Outcomes and Measures\\textless/h3\\textgreater\\textlessp\\textgreaterChange in HIV viral suppression (<75 copies/mL) over a 12-month period.\\textless/p\\textgreater\\textlessh3\\textgreaterInterventions\\textless/h3\\textgreater\\textlessp\\textgreaterDuring the 12-session, 24-week LINK LA Peer Navigation intervention, trained peer navigators counseled participants on goal setting and problem solving around barriers to HIV care and adherence, starting while the participants were still in jail. After their release, they continued counseling while they accompanied participants to 2 HIV care visits, then facilitated communication with clinicians during visits.\\textless/p\\textgreater\\textlessh3\\textgreaterResults\\textless/h3\\textgreater\\textlessp\\textgreaterOf 356 participants randomized, 151 (42%) were black; 110 (31%) were Latino; 303 (85%) were men; 53 (15%) were transgender women; and the mean (SD) age was 39.5 (10.4) years. At 12 months, viral suppression was achieved by 62 (49.6%) of 125 participants in the peer navigation (intervention) arm compared with 45 (36.0%) of 125 in the transitional case management (control) arm, for an unadjusted treatment difference of 13.6% (95% CI, 1.34%-25.9%;P = .03). In the repeated measures, random effects, logistic model the adjusted probability of viral suppression declined from 52% at baseline to 30% among controls, while those in the peer navigation arm maintained viral suppression at 49% from baseline to 12 months, for a difference-in-difference of 22% (95% CI, 0.03-0.41;P = .02).\\textless/p\\textgreater\\textlessh3\\textgreaterConclusions and Relevance\\textless/h3\\textgreater\\textlessp\\textgreaterThe LINK LA peer navigation intervention was successful at preventing declines in viral suppression, typically seen after release from incarceration, compared with standard transitional case management. Future research should examine ways to strengthen the intervention to increase viral suppression above baseline levels.\\textless/p\\textgreater\\textlessh3\\textgreaterTrial Registration\\textless/h3\\textgreater\\textlessp\\textgreaterclinicaltrials.gov Identifier:NCT01406626\\textless/p\\textgreater\n

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\n \n\n \n \n Springer, S. A.; Di Paola, A.; Azar, M. M.; Barbour, R.; Biondi, B. E.; Desabrais, M.; Lincoln, T.; Skiest, D. J.; and Altice, F. L.\n\n\n \n \n \n \n \n Extended-Release Naltrexone Improves Viral Suppression Among Incarcerated Persons Living With HIV With Opioid Use Disorders Transitioning to the Community: Results of a Double-Blind, Placebo-Controlled Randomized Trial.\n \n \n \n \n\n\n \n\n\n\n JAIDS Journal of Acquired Immune Deficiency Syndromes, 78(1): 43. May 2018.\n \n\n\n\n
\n\n\n\n \n \n $\"Extended-Release$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{springer_extended-release_2018,\n\ttitle = {Extended-{Release} {Naltrexone} {Improves} {Viral} {Suppression} {Among} {Incarcerated} {Persons} {Living} {With} {HIV} {With} {Opioid} {Use} {Disorders} {Transitioning} to the {Community}: {Results} of a {Double}-{Blind}, {Placebo}-{Controlled} {Randomized} {Trial}},\n\tvolume = {78},\n\tissn = {1525-4135},\n\tshorttitle = {Extended-{Release} {Naltrexone} {Improves} {Viral} {Suppression} {Among} {Incarcerated} {Persons} {Living} {With} {HIV} {With} {Opioid} {Use} {Disorders} {Transitioning} to the {Community}},\n\turl = {https://journals.lww.com/jaids/Abstract/2018/05010/Extended_Release_Naltrexone_Improves_Viral.7.aspx},\n\tdoi = {10.1097/QAI.0000000000001634},\n\tabstract = {Objective: To determine whether extended-release naltrexone (XR-NTX) would improve or maintain viral suppression (VS) among prisoners or jail detainees with HIV and opioid use disorder (OUD) transitioning to the community.\n        Design: A 4-site, prospective randomized double-blind, placebo-controlled trial was conducted among prison and jail inmates with HIV and OUD transitioning to the community from September 2010 through March 2016.\n        Methods: Eligible participants (N = 93) were randomized 2:1 to receive 6 monthly injections of XR-NTX (n = 66) or placebo (n = 27) starting at release and observed for 6 months. The primary outcome was the proportion that maintained or improved VS ({\\textless}50 copies/mL) from baseline to 6 months.\n        Results: Participants allocated to XR-NTX significantly improved to VS ({\\textless}50 copies/mL) from baseline (37.9\\%) to 6 months (60.6\\%) (P = 0.002), whereas the placebo group did not (55.6\\% at baseline to 40.7\\% at 6 months P = 0.294). There was, however, no statistical significant difference in VS levels at 6 months between XR-NTX (60.6\\%) vs. placebo (40.7\\%) (P = 0.087). After controlling for other factors, only allocation to XR-NTX (adjusted odds ratio = 2.90; 95\\% confidence interval = 1.04 to 8.14, P = 0.043) was associated with the primary outcome. Trajectories in VS from baseline to 6 months differed significantly (P = 0.017) between treatment groups, and the differences in the discordant values were significantly different as well (P = 0.041): the XR-NTX group was more likely than the placebo group to improve VS (30.3\\% vs. 18.5\\%), maintain VS (30.3\\% vs. 27.3), and less likely to lose VS (7.6\\% vs. 33.3\\%) by 6 months.\n        Conclusions: XR-NTX improves or maintains VS after release to the community for incarcerated people living with HIV with OUD.},\n\tlanguage = {en-US},\n\tnumber = {1},\n\turldate = {2018-04-25},\n\tjournal = {JAIDS Journal of Acquired Immune Deficiency Syndromes},\n\tauthor = {Springer, Sandra A. and Di Paola, Angela and Azar, Marwan M. and Barbour, Russell and Biondi, Breanne E. and Desabrais, Maureen and Lincoln, Thomas and Skiest, Daniel J. and Altice, Frederick L.},\n\tmonth = may,\n\tyear = {2018},\n\tpages = {43},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Christopoulos, K. A.; Riley, E. D.; Carrico, A. W.; Tulsky, J.; Moskowitz, J. T.; Dilworth, S.; Coffin, L. S.; Wilson, L.; Peretz, J. J.; and Hilton, J. F.\n\n\n \n \n \n \n \n A Randomized Controlled Trial of a Text Messaging Intervention to Promote Virologic Suppression and Retention in Care in an Urban Safety-Net HIV Clinic: The Connect4Care (C4C) Trial.\n \n \n \n \n\n\n \n\n\n\n Clinical Infectious Diseases. February 2018.\n \n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{christopoulos_randomized_2018,\n\ttitle = {A {Randomized} {Controlled} {Trial} of a {Text} {Messaging} {Intervention} to {Promote} {Virologic} {Suppression} and {Retention} in {Care} in an {Urban} {Safety}-{Net} {HIV} {Clinic}: {The} {Connect4Care} ({C4C}) {Trial}},\n\tshorttitle = {A {Randomized} {Controlled} {Trial} of a {Text} {Messaging} {Intervention} to {Promote} {Virologic} {Suppression} and {Retention} in {Care} in an {Urban} {Safety}-{Net} {HIV} {Clinic}},\n\turl = {https://academic.oup.com/cid/advance-article/doi/10.1093/cid/ciy156/4883333},\n\tdoi = {10.1093/cid/ciy156},\n\tabstract = {BackgroundText messaging is a promising strategy to support HIV care engagement, but little is known about its efficacy in urban safety-net HIV clinic populations.MethodsWe conducted a randomized controlled trial of a supportive and motivational text messaging intervention, Connect4Care (C4C), among viremic patients who had a history of poor retention or were new to clinic. Participants were randomized (stratified by new HIV diagnosis status) to receive one of the following for 12 months: 1) thrice-weekly intervention messages, plus texted primary care appointment reminders and a monthly text message requesting confirmation of study participation, or; 2) texted reminders and monthly messages alone. Viral load was assessed at 6 and 12 months. The primary outcome was virologic suppression (\\&lt;200 copies/mL) at 12 months, estimated via repeated measures log-binomial regression, adjusted for new diagnosis status. The secondary outcome was retention in clinic care.ResultsBetween August 2013-November 2015, 230 participants were randomized. Virologic suppression at 12 months was similar between intervention and control participants (48.8\\% vs. 45.8\\%), with negligible change from 6-month estimates, yielding RR 1.07 (95\\% CI: 0.82, 1.39). Suppression was higher in the newly diagnosed (78.3\\% vs. 45.3\\%). There were no intervention effects on the secondary outcome. Exploratory analyses suggested that patients with more responses to study text messages had better outcomes, regardless of arm.ConclusionsThe C4C text messaging intervention did not significantly increase virologic suppression or retention in care. Response to text messages may be a useful way for providers to gauge risk for poor HIV outcomes.Clinical Trials RegistrationNCT01917994},\n\tlanguage = {en},\n\turldate = {2018-03-19},\n\tjournal = {Clinical Infectious Diseases},\n\tauthor = {Christopoulos, Katerina A. and Riley, Elise D. and Carrico, Adam W. and Tulsky, Jacqueline and Moskowitz, Judith T. and Dilworth, Samantha and Coffin, Lara S. and Wilson, Leslie and Peretz, Jason Johnson and Hilton, Joan F.},\n\tmonth = feb,\n\tyear = {2018},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Mbaba, M.; Brown, S.; Wooditch, A.; Kiss, M.; Murphy, A.; Kumari, S.; Taxman, F.; Altice, F.; Lawson, W. B.; and Springer, S. A.\n\n\n \n \n \n \n \n Prevalence, Diagnosis, and Treatment Rates of Mood Disorders among Opioid Users under Criminal Justice Supervision.\n \n \n \n \n\n\n \n\n\n\n Substance Use & Misuse,1–10. January 2018.\n \n\n\n\n
\n\n\n\n \n \n $\"Prevalence,$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{mbaba_prevalence_2018,\n\ttitle = {Prevalence, {Diagnosis}, and {Treatment} {Rates} of {Mood} {Disorders} among {Opioid} {Users} under {Criminal} {Justice} {Supervision}},\n\tissn = {1532-2491},\n\turl = {http://www.tandfonline.com/doi/full/10.1080/10826084.2017.1416400},\n\tdoi = {10.1080/10826084.2017.1416400},\n\tlanguage = {eng},\n\tjournal = {Substance Use \\& Misuse},\n\tauthor = {Mbaba, Mary and Brown, Shan-Estelle and Wooditch, Alese and Kiss, Marissa and Murphy, Amy and Kumari, Suneeta and Taxman, Faye and Altice, Frederick and Lawson, William B. and Springer, Sandra A.},\n\tmonth = jan,\n\tyear = {2018},\n\tpmid = {29333954},\n\tkeywords = {Mood disorder, bipolar, buprenorphine, criminal justice, depression, heroin, mental health treatment, opioid},\n\tpages = {1--10},\n}\n\n\n\n\n\n\n\n

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\n \n 2017\n \n \n (23)\n \n \n

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\n \n\n \n \n MCFALL, A. M.; SOLOMON, S. S.; LUCAS, G. M.; CELENTANO, D. D.; SRIKRISHNAN, A. K.; KUMAR, M. S.; and MEHTA, S. H.\n\n\n \n \n \n \n \n Epidemiology of HIV and hepatitis C infection among women who inject drugs in Northeast India: A respondent-driven sampling study.\n \n \n \n \n\n\n \n\n\n\n Addiction (Abingdon, England), 112(8): 1480–1487. April 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Epidemiology$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{mcfall_epidemiology_2017,\n\ttitle = {Epidemiology of {HIV} and hepatitis {C} infection among women who inject drugs in {Northeast} {India}: {A} respondent-driven sampling study},\n\tvolume = {112},\n\tissn = {0965-2140},\n\tshorttitle = {Epidemiology of {HIV} and hepatitis {C} infection among women who inject drugs in {Northeast} {India}},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5503783/},\n\tdoi = {10.1111/add.13821},\n\tabstract = {Background and aims\nDespite extensive research on HIV and hepatitis C (HCV) among people who inject drugs (PWID), there remains a gap in knowledge on the burden among women who inject drugs and their unique contexts and risk factors. This analysis compares HIV and HCV prevalence in female and male PWID and estimates injection and sexual risk correlates of prevalent HIV and HCV infection among women in Northeast India.\n\nDesign\nCross-sectional sample accrued using respondent-driven sampling.\n\nSetting\nSeven cities in Northeast India, 2013.\n\nParticipants\n6,457 adult PWID.\n\nMeasurements\nParticipants completed an interviewer-administered survey. HIV infection was diagnosed onsite and HCV antibody testing was done on stored specimens. HIV and HCV prevalence estimates were stratified by gender. Among women, the association of risk correlates with HIV and HCV were estimated using multi-level logistic regression models.\n\nFindings\n796 (16\\%) of the PWID were women, of whom 53\\% (95\\% confidence interval [CI]: 49–57\\%) were HIV-infected and 22\\% (CI: 20–25\\%) were HCV-infected. HIV and HCV prevalence among men was 17\\% (CI: 17–18\\%) and 32\\% (CI: 31–32\\%), respectively. Among women, correlates of HIV were widowhood (adjusted odds ratio [aOR] vs. currently married: 4.0, CI: 2.1–7.6) and a higher number of lifetime sexual partners (aOR ≥8 vs. none: 3.1, CI: 1.1–8.9). Correlates of HCV were longer injection duration (aOR per 10 years: 1.7, CI: 1.3–2.3), injecting only heroin and a combination of drugs (aOR vs. pharmaceuticals only: 5.6, CI: 1.7–18.9 and aOR: 2.6, CI: 1.6–4.2, respectively), sharing needles/syringes (aOR: 2.5, CI: 1.3–4.6) and a larger PWID network (aOR ≥51 vs. 1–5: 4.2, CI: 2.4–7.2).\n\nConclusions\nWomen who inject drugs in Northeast India have a high HIV prevalence which was more than double their hepatitis C (HCV) prevalence, an opposite pattern than is typically observed among male PWID. HIV infection is associated with sexual risk factors while injection-related behaviors appear to drive HCV infection.},\n\tnumber = {8},\n\turldate = {2018-11-20},\n\tjournal = {Addiction (Abingdon, England)},\n\tauthor = {MCFALL, Allison M. and SOLOMON, Sunil S. and LUCAS, Greg M. and CELENTANO, David D. and SRIKRISHNAN, Aylur K. and KUMAR, Muniratnam S. and MEHTA, Shruti H.},\n\tmonth = apr,\n\tyear = {2017},\n\tpmid = {28317210},\n\tpmcid = {PMC5503783},\n\tpages = {1480--1487},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n Background and aims Despite extensive research on HIV and hepatitis C (HCV) among people who inject drugs (PWID), there remains a gap in knowledge on the burden among women who inject drugs and their unique contexts and risk factors. This analysis compares HIV and HCV prevalence in female and male PWID and estimates injection and sexual risk correlates of prevalent HIV and HCV infection among women in Northeast India. Design Cross-sectional sample accrued using respondent-driven sampling. Setting Seven cities in Northeast India, 2013. Participants 6,457 adult PWID. Measurements Participants completed an interviewer-administered survey. HIV infection was diagnosed onsite and HCV antibody testing was done on stored specimens. HIV and HCV prevalence estimates were stratified by gender. Among women, the association of risk correlates with HIV and HCV were estimated using multi-level logistic regression models. Findings 796 (16%) of the PWID were women, of whom 53% (95% confidence interval [CI]: 49–57%) were HIV-infected and 22% (CI: 20–25%) were HCV-infected. HIV and HCV prevalence among men was 17% (CI: 17–18%) and 32% (CI: 31–32%), respectively. Among women, correlates of HIV were widowhood (adjusted odds ratio [aOR] vs. currently married: 4.0, CI: 2.1–7.6) and a higher number of lifetime sexual partners (aOR ≥8 vs. none: 3.1, CI: 1.1–8.9). Correlates of HCV were longer injection duration (aOR per 10 years: 1.7, CI: 1.3–2.3), injecting only heroin and a combination of drugs (aOR vs. pharmaceuticals only: 5.6, CI: 1.7–18.9 and aOR: 2.6, CI: 1.6–4.2, respectively), sharing needles/syringes (aOR: 2.5, CI: 1.3–4.6) and a larger PWID network (aOR ≥51 vs. 1–5: 4.2, CI: 2.4–7.2). Conclusions Women who inject drugs in Northeast India have a high HIV prevalence which was more than double their hepatitis C (HCV) prevalence, an opposite pattern than is typically observed among male PWID. HIV infection is associated with sexual risk factors while injection-related behaviors appear to drive HCV infection.\n

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\n \n\n \n \n Cepeda, J. A.; Solomon, S. S.; Srikrishnan, A. K.; McFall, A. M.; Kumar, M. S.; Vasudevan, C. K.; Anand, S.; Celentano, D. D.; Lucas, G. M.; and Mehta, S. H.\n\n\n \n \n \n \n \n Injection drug network characteristics are important markers of HIV risk behavior and lack of viral suppression.\n \n \n \n \n\n\n \n\n\n\n Journal of acquired immune deficiency syndromes (1999), 75(3): 257–264. July 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Injection$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{cepeda_injection_2017,\n\ttitle = {Injection drug network characteristics are important markers of {HIV} risk behavior and lack of viral suppression},\n\tvolume = {75},\n\tissn = {1525-4135},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5472484/},\n\tdoi = {10.1097/QAI.0000000000001372},\n\tabstract = {Background\nPeople who inject drugs (PWID) who are highly connected within their injection drug networks may be important HIV transmission nodes if they frequently share syringes with other PWID and are not engaged in HIV care. In India, HIV transmission fueled by injection drug use is increasing, however little is known about the associations between injection network size and syringe sharing and viral suppression.\n\nMethods\nWe recruited 14,481 PWID between October 2012 – December 2013 by respondent driven sampling across 15 sites in India. Interviewer-administered questionnaires assessed network characteristics, substance use, HIV testing experience, and access to health services. We used multilevel logistic regression modeling to evaluate the relationship between injection drug network size and 1) syringe sharing at last injection and 2) viral suppression among HIV-positive participants ({\\textless}150 copies/ml).\n\nFindings\nThe median injection network size was 3 [IQR: 1–5] and 7\\% of participants injected with {\\textgreater}10 members in the past 30 days. PWID who had {\\textgreater}10 members in their network were 1.65 times (95\\% CI: 1.12 – 2.42, p=0.0111) more likely to have shared a syringe at last injection compared to those in the 0–1 members in their drug networks. Additionally, individuals with the largest injection drug networks were also 31\\% (95\\% CI: 0.53 – 0.90, p=0.006) less likely to be virally suppressed compared to individuals in the smallest injection drug networks.\n\nDiscussion\nIndividuals with larger networks may be important in HIV transmission within injection drug networks since they were the most likely to engage in recent syringe sharing and least likely to be virally suppressed.},\n\tnumber = {3},\n\turldate = {2018-11-20},\n\tjournal = {Journal of acquired immune deficiency syndromes (1999)},\n\tauthor = {Cepeda, Javier A. and Solomon, Sunil S. and Srikrishnan, Aylur K. and McFall, Allison M. and Kumar, M. Suresh and Vasudevan, Canjeevaram K. and Anand, Santhanam and Celentano, David D. and Lucas, Gregory M. and Mehta, Shruti H.},\n\tmonth = jul,\n\tyear = {2017},\n\tpmid = {28328550},\n\tpmcid = {PMC5472484},\n\tpages = {257--264},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Christopoulos, K. A.; Cunningham, W. E.; Beckwith, C. G.; Kuo, I.; Golin, C. E.; Knight, K.; Flynn, P. M.; Spaulding, A. C.; Coffin, L. S.; Kruszka, B.; Kurth, A.; Young, J. D.; Mannheimer, S.; Crane, H. M.; and Kahana, S. Y.\n\n\n \n \n \n \n \n Implementation of Seek, Test, Treat, Retain Interventions Using Mobile Phones and Text Messaging to Improve Engagement in HIV Care for Vulnerable Populations in the United States.\n \n \n \n \n\n\n \n\n\n\n AIDS and behavior, 21(11): 3182–3193. November 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Implementation$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n\n\n\n

@article{christopoulos_implementation_2017,\n\ttitle = {Implementation of {Seek}, {Test}, {Treat}, {Retain} {Interventions} {Using} {Mobile} {Phones} and {Text} {Messaging} to {Improve} {Engagement} in {HIV} {Care} for {Vulnerable} {Populations} in the {United} {States}},\n\tvolume = {21},\n\tissn = {1090-7165},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5669804/},\n\tdoi = {10.1007/s10461-017-1804-8},\n\tabstract = {In the United States, little is known about interventions that rely on mobile phones and/or text messaging to improve engagement in HIV care for vulnerable populations. Domestic studies using these technologies as part of the National Institute on Drug Abuse “Seek, Test, Treat, Retain” research initiative were queried regarding intervention components, implementation issues, participant characteristics, and descriptive statistics of mobile phone service delivery. Across five studies with 1,135 predominantly male, minority participants, implementation challenges occurred in three categories: 1) service interruptions; 2) billing/overage issues, and; 3) the participant user experience. Response rules for automated text messages frequently frustrated participants. The inability to reload minutes/texting capacity remotely was a significant barrier to intervention delivery. No study encountered confidentiality breaches. Service interruption was common, even if studies provided mobile phones and plans. Future studies should attend to the type of mobile phone and service, the participant user experience, and human subjects concerns.},\n\tnumber = {11},\n\turldate = {2018-11-20},\n\tjournal = {AIDS and behavior},\n\tauthor = {Christopoulos, Katerina A. and Cunningham, William E. and Beckwith, Curt G. and Kuo, Irene and Golin, Carol E. and Knight, Kevin and Flynn, Patrick M. and Spaulding, Anne C. and Coffin, Lara S. and Kruszka, Bridget and Kurth, Ann and Young, Jeremy D. and Mannheimer, Sharon and Crane, Heidi M. and Kahana, Shoshana Y.},\n\tmonth = nov,\n\tyear = {2017},\n\tpmid = {28578543},\n\tpmcid = {PMC5669804},\n\tkeywords = {STTR Core},\n\tpages = {3182--3193},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Loeliger, K. B.; Biggs, M. L.; Young, R.; Seal, D. W.; Beckwith, C. G.; Kuo, I.; Gordon, M. S.; Altice, F. L.; Ouellet, L. J.; Cunningham, W. E.; Young, J. D.; and Springer, S. A.\n\n\n \n \n \n \n \n Gender Differences in HIV Risk Behaviors Among Persons Involved in the U.S. Criminal Justice System and Living with HIV or at Risk for HIV: A “Seek, Test, Treat, and Retain” Harmonization Consortium.\n \n \n \n \n\n\n \n\n\n\n AIDS and behavior, 21(10): 2945–2957. October 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Gender$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n\n\n\n

@article{loeliger_gender_2017,\n\ttitle = {Gender {Differences} in {HIV} {Risk} {Behaviors} {Among} {Persons} {Involved} in the {U}.{S}. {Criminal} {Justice} {System} and {Living} with {HIV} or at {Risk} for {HIV}: {A} “{Seek}, {Test}, {Treat}, and {Retain}” {Harmonization} {Consortium}},\n\tvolume = {21},\n\tissn = {1090-7165},\n\tshorttitle = {Gender {Differences} in {HIV} {Risk} {Behaviors} {Among} {Persons} {Involved} in the {U}.{S}. {Criminal} {Justice} {System} and {Living} with {HIV} or at {Risk} for {HIV}},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5552433/},\n\tdoi = {10.1007/s10461-017-1722-9},\n\tabstract = {The U.S. female criminal justice (CJ) population is rapidly growing, yet large-scale studies exploring gender-specific HIV risk behaviors in the CJ population are lacking. This analysis uses baseline data on adults with a CJ history from eight U.S. studies in an NIH-funded “Seek, Test, Treat, Retain” harmonization consortium. Data were collected using a standardized HIV risk behavior assessment tool and pooled across studies to describe participants’ characteristics and risk behaviors. Multilevel mixed-effects logistic regression models were used to test for gender-based behavior differences. Among 784 HIV-positive (21.4\\% female) and 5521 HIV-negative (8.5\\% female) participants, HIV-positive women had higher odds than HIV-positive men of engaging in condomless sexual intercourse (AOR 1.84 [1.16–2.95]) with potentially sero-discordant partners (AOR 2.40 [1.41–4.09]) and of sharing injection equipment (AOR 3.36 [1.31–8.63]). HIV risk reduction interventions targeting CJ-involved women with HIV are urgently needed as this population may represent an under-recognized potential source of HIV transmission.},\n\tnumber = {10},\n\turldate = {2018-06-21},\n\tjournal = {AIDS and behavior},\n\tauthor = {Loeliger, Kelsey B. and Biggs, Mary L. and Young, Rebekah and Seal, David W. and Beckwith, Curt G. and Kuo, Irene and Gordon, Michael S. and Altice, Frederick L. and Ouellet, Lawrence J. and Cunningham, William E. and Young, Jeremy D. and Springer, Sandra A.},\n\tmonth = oct,\n\tyear = {2017},\n\tpmid = {28188460},\n\tpmcid = {PMC5552433},\n\tkeywords = {STTR Core},\n\tpages = {2945--2957},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Harawa, N. T.; Amani, B.; Bowers, J. R.; Sayles, J. N.; and Cunningham, W.\n\n\n \n \n \n \n \n Understanding Interactions of Formerly Incarcerated HIV-Positive Men and Transgender Women with Addiction Treatment, Medical, and Criminal Justice Systems.\n \n \n \n \n\n\n \n\n\n\n The International journal on drug policy, 48: 63–71. August 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Understanding$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{harawa_understanding_2017,\n\ttitle = {Understanding {Interactions} of {Formerly} {Incarcerated} {HIV}-{Positive} {Men} and {Transgender} {Women} with {Addiction} {Treatment}, {Medical}, and {Criminal} {Justice} {Systems}},\n\tvolume = {48},\n\tissn = {0955-3959},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5620016/},\n\tdoi = {10.1016/j.drugpo.2017.05.013},\n\tabstract = {Background\nLow levels of medical care engagement have been noted for HIV-positive people leaving systems of incarceration in the United States. Substance misuse frequently co-occurs with criminal justice involvement in individuals who are living with HIV.\n\nMethods\nWe analyzed data from in-depth interviews with 19 HIV-positive individuals who were currently or formerly incarcerated in order to elucidate challenges faced in accessing care and maintaining HIV treatment regimens when cycling out of (and often back into) custody. Our thematic analysis used an ecosocial framework to describe participants’ shifts between substance abuse treatment, medical care, and criminal justice systems.\n\nResults\nDominant themes included the dramatic increase in HIV-treatment-related autonomy required following release from jail because of differences in care delivery between custody-based and community-based care systems; the important, but temporary stabilization provided by residential substance abuse treatment programs; and the inconsistency of substance abuse treatment approaches with chronic care models of disease management.\n\nConclusions\nEnhanced integration of criminal justice, medical care, and substance abuse treatment institutions in planning for reentry of HIV populations may ease the impact of the dramatic shifts in context that often dissuade linkage and retention. This integration should include coordination with custody release processes, periodic assessments for active substance misuse in HIV treatment settings, support for (re)establishing health-promoting social networks, and options for long-term, residential substance abuse treatment programs.},\n\turldate = {2018-06-21},\n\tjournal = {The International journal on drug policy},\n\tauthor = {Harawa, Nina T. and Amani, Bita and Bowers, Jane Rohde and Sayles, Jennifer N. and Cunningham, William},\n\tmonth = aug,\n\tyear = {2017},\n\tpmid = {28804052},\n\tpmcid = {PMC5620016},\n\tpages = {63--71},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Wechsberg, W. M.; van der Horst, C.; Ndirangu, J.; Doherty, I. A.; Kline, T.; Browne, F. A.; Belus, J. M.; Nance, R.; and Zule, W. A.\n\n\n \n \n \n \n \n Seek, test, treat: substance-using women in the HIV treatment cascade in South Africa.\n \n \n \n \n\n\n \n\n\n\n Addiction Science & Clinical Practice, 12. April 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Seek,$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{wechsberg_seek_2017,\n\ttitle = {Seek, test, treat: substance-using women in the {HIV} treatment cascade in {South} {Africa}},\n\tvolume = {12},\n\tissn = {1940-0632},\n\tshorttitle = {Seek, test, treat},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5405464/},\n\tdoi = {10.1186/s13722-017-0077-x},\n\tabstract = {Background\nWomen in South Africa who use alcohol and other drugs face multiple barriers to HIV care. These barriers make it difficult for women to progress through each step in the HIV treatment cascade from diagnosis to treatment initiation and adherence. This paper examines correlates of HIV status, newly diagnosed HIV status, and use of antiretroviral therapy (ART).\n\nMethods\nOutreach workers recruited sexually active Black African women who used substances in Pretoria as part of a U.S. National Institutes of Health-funded geographically clustered randomized trial examining the effect of an intervention to reduce alcohol and drug use as well as sexual risk behaviors. To address the question of interest in the current investigation, cross-sectional baseline data were used. At study enrollment, all participants (N = 641) completed an interview, and underwent rapid HIV testing and biological drug screening. Those who tested positive for HIV and were eligible for ART were asked about their barriers to initiating or adhering to ART. Bivariate and multivariable logistic regression analyses were conducted to determine correlates of HIV status, newly diagnosed HIV, and ART use.\n\nResults\nAt enrollment, 55\\% of participants tested positive for HIV, and 36\\% of these women were newly diagnosed. In multivariable analyses of the entire sample, women who had completed 10th grade were less likely to be living with HIV (OR 0.69; CI 0.48, 0.99) and those from the inner city were more likely to be living with HIV (OR 1.83; CI 1.26, 2.67). Among HIV-positive participants, women were less likely to be newly diagnosed if they had ever been in substance abuse treatment (OR 0.15; CI 0.03, 0.69) or used a condom at last sex (OR 0.58; CI 0.34, 0.98) and more likely to be newly diagnosed if they were physically assaulted in the past year (OR 1.97; CI 1.01, 3.84). Among women eligible for ART, fewer were likely to be on treatment (by self-report) if they had a positive urine test for opiates or cocaine (OR 0.27; CI 0.09, 0.80).\n\nConclusions\nThese results, although cross-sectional, provide some guidance for provincial authorities to address barriers to HIV care for sexually active, substance-using vulnerable women in Pretoria. Targeting the inner city with prevention campaigns, expanding and improving substance abuse treatment programs, linking clients with simultaneous HIV testing and treatment, and targeting women who have experienced sexual assault and violence may help the government achieve the UNAIDS 90-90-90 treatment target., Clinical Trials.gov NCT01497405 registered on December 1, 2011.},\n\turldate = {2018-06-21},\n\tjournal = {Addiction Science \\& Clinical Practice},\n\tauthor = {Wechsberg, Wendee M. and van der Horst, Charles and Ndirangu, Jacqueline and Doherty, Irene A. and Kline, Tracy and Browne, Felicia A. and Belus, Jennifer M. and Nance, Robin and Zule, William A.},\n\tmonth = apr,\n\tyear = {2017},\n\tpmid = {28441975},\n\tpmcid = {PMC5405464},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n Background Women in South Africa who use alcohol and other drugs face multiple barriers to HIV care. These barriers make it difficult for women to progress through each step in the HIV treatment cascade from diagnosis to treatment initiation and adherence. This paper examines correlates of HIV status, newly diagnosed HIV status, and use of antiretroviral therapy (ART). Methods Outreach workers recruited sexually active Black African women who used substances in Pretoria as part of a U.S. National Institutes of Health-funded geographically clustered randomized trial examining the effect of an intervention to reduce alcohol and drug use as well as sexual risk behaviors. To address the question of interest in the current investigation, cross-sectional baseline data were used. At study enrollment, all participants (N = 641) completed an interview, and underwent rapid HIV testing and biological drug screening. Those who tested positive for HIV and were eligible for ART were asked about their barriers to initiating or adhering to ART. Bivariate and multivariable logistic regression analyses were conducted to determine correlates of HIV status, newly diagnosed HIV, and ART use. Results At enrollment, 55% of participants tested positive for HIV, and 36% of these women were newly diagnosed. In multivariable analyses of the entire sample, women who had completed 10th grade were less likely to be living with HIV (OR 0.69; CI 0.48, 0.99) and those from the inner city were more likely to be living with HIV (OR 1.83; CI 1.26, 2.67). Among HIV-positive participants, women were less likely to be newly diagnosed if they had ever been in substance abuse treatment (OR 0.15; CI 0.03, 0.69) or used a condom at last sex (OR 0.58; CI 0.34, 0.98) and more likely to be newly diagnosed if they were physically assaulted in the past year (OR 1.97; CI 1.01, 3.84). Among women eligible for ART, fewer were likely to be on treatment (by self-report) if they had a positive urine test for opiates or cocaine (OR 0.27; CI 0.09, 0.80). Conclusions These results, although cross-sectional, provide some guidance for provincial authorities to address barriers to HIV care for sexually active, substance-using vulnerable women in Pretoria. Targeting the inner city with prevention campaigns, expanding and improving substance abuse treatment programs, linking clients with simultaneous HIV testing and treatment, and targeting women who have experienced sexual assault and violence may help the government achieve the UNAIDS 90-90-90 treatment target., Clinical Trials.gov NCT01497405 registered on December 1, 2011.\n

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\n \n\n \n \n Wohl, D. A.; Golin, C. E; Knight, K.; Gould, M.; Carda-Auten, J.; Groves, J. S; Napravnik, S.; Cole, S. R; White, B. L; Fogel, C.; Rosen, D. L; Mugavaro, M. J; Pence, B. W; and Flynn, P. M\n\n\n \n \n \n \n \n A Randomized Controlled Trial of an Intervention to Maintain Suppression of HIV Viremia Following Prison Release: The imPACT Trial - JAIDS Ms. No.: QAIV16986.\n \n \n \n \n\n\n \n\n\n\n Journal of acquired immune deficiency syndromes (1999), 75(1): 81–90. May 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{wohl_randomized_2017,\n\ttitle = {A {Randomized} {Controlled} {Trial} of an {Intervention} to {Maintain} {Suppression} of {HIV} {Viremia} {Following} {Prison} {Release}: {The} {imPACT} {Trial} - {JAIDS} {Ms}. {No}.: {QAIV16986}},\n\tvolume = {75},\n\tissn = {1525-4135},\n\tshorttitle = {A {Randomized} {Controlled} {Trial} of an {Intervention} to {Maintain} {Suppression} of {HIV} {Viremia} {Following} {Prison} {Release}},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5443668/},\n\tdoi = {10.1097/QAI.0000000000001337},\n\tabstract = {Background\nHIV-infected individuals transitioning from incarceration to the community are at risk for loss of viral suppression. We compared the effects of imPACT, a multi-dimensional intervention to promote care engagement after release, to standard care on sustaining viral suppression after community re-entry.\n\nMethods\nThis trial randomized 405 HIV-infected inmates being released from prisons in Texas and North Carolina with HIV-1 RNA levels {\\textless}400 copies/mL to imPACT versus standard care. The imPACT arm received motivational interviewing pre- and post-release, referral to care within 5 days of release, and a cellphone for medication text reminders. The standard care arm received routine discharge planning and a cellphone for study staff contact. The primary outcome was the difference between arms in week 24 post-release viral suppression (HIV-1 RNA {\\textless}50 copies/mL) using intent-to-treat analysis with multiple imputation of missing data.\n\nResults\nThe proportion with 24-week HIV-1 RNA {\\textless}50 copies/ml was 60\\% and 61\\% in the imPACT and standard care arms, respectively (odds ratio for suppression 0.95 (95\\% CI, 0.59 to 1.53)). By week 6 post-release, 86\\% in the imPACT arm versus 75\\% in the standard care arm attended at least one non-emergency clinic visit (P = 0.02). At week 24, 62\\% in both arms reported not missing any antiretroviral doses in the past 30 days (P {\\textgreater}0.99).\n\nConclusions\nHigher rates of HIV suppression and medical care engagement than expected based on prior literature were observed among HIV-infected patients with suppressed viremia released from prison. Randomization to a comprehensive intervention to motivate and facilitate HIV care access after prison release did not prevent loss of viral suppression. A better understanding of the factors influencing prison releasees' linkage to community care, medication adherence, and maintenance of viral suppression is needed to inform policy and other strategic approaches to HIV prevention and treatment.},\n\tnumber = {1},\n\turldate = {2018-06-21},\n\tjournal = {Journal of acquired immune deficiency syndromes (1999)},\n\tauthor = {Wohl, David Alain and Golin, Carol E and Knight, Kevin and Gould, Michele and Carda-Auten, Jessica and Groves, Jennifer S and Napravnik, Sonia and Cole, Stephen R and White, Becky L and Fogel, Cathie and Rosen, David L and Mugavaro, Michael J and Pence, Brian W and Flynn, Patrick M},\n\tmonth = may,\n\tyear = {2017},\n\tpmid = {28277487},\n\tpmcid = {PMC5443668},\n\tpages = {81--90},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n Background HIV-infected individuals transitioning from incarceration to the community are at risk for loss of viral suppression. We compared the effects of imPACT, a multi-dimensional intervention to promote care engagement after release, to standard care on sustaining viral suppression after community re-entry. Methods This trial randomized 405 HIV-infected inmates being released from prisons in Texas and North Carolina with HIV-1 RNA levels \\textless400 copies/mL to imPACT versus standard care. The imPACT arm received motivational interviewing pre- and post-release, referral to care within 5 days of release, and a cellphone for medication text reminders. The standard care arm received routine discharge planning and a cellphone for study staff contact. The primary outcome was the difference between arms in week 24 post-release viral suppression (HIV-1 RNA \\textless50 copies/mL) using intent-to-treat analysis with multiple imputation of missing data. Results The proportion with 24-week HIV-1 RNA \\textless50 copies/ml was 60% and 61% in the imPACT and standard care arms, respectively (odds ratio for suppression 0.95 (95% CI, 0.59 to 1.53)). By week 6 post-release, 86% in the imPACT arm versus 75% in the standard care arm attended at least one non-emergency clinic visit (P = 0.02). At week 24, 62% in both arms reported not missing any antiretroviral doses in the past 30 days (P \\textgreater0.99). Conclusions Higher rates of HIV suppression and medical care engagement than expected based on prior literature were observed among HIV-infected patients with suppressed viremia released from prison. Randomization to a comprehensive intervention to motivate and facilitate HIV care access after prison release did not prevent loss of viral suppression. A better understanding of the factors influencing prison releasees' linkage to community care, medication adherence, and maintenance of viral suppression is needed to inform policy and other strategic approaches to HIV prevention and treatment.\n

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\n \n\n \n \n Cleland, C. M.; Lanza, S. T.; Vasilenko, S. A.; and Gwadz, M.\n\n\n \n \n \n \n \n Syndemic Risk Classes and Substance Use Problems among Adults in High-Risk Urban Areas: A Latent Class Analysis.\n \n \n \n \n\n\n \n\n\n\n Frontiers in Public Health, 5. September 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Syndemic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{cleland_syndemic_2017,\n\ttitle = {Syndemic {Risk} {Classes} and {Substance} {Use} {Problems} among {Adults} in {High}-{Risk} {Urban} {Areas}: {A} {Latent} {Class} {Analysis}},\n\tvolume = {5},\n\tissn = {2296-2565},\n\tshorttitle = {Syndemic {Risk} {Classes} and {Substance} {Use} {Problems} among {Adults} in {High}-{Risk} {Urban} {Areas}},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5594078/},\n\tdoi = {10.3389/fpubh.2017.00237},\n\tabstract = {Substance use problems tend to co-occur with risk factors that are especially prevalent in urban communities with high rates of poverty. The present study draws on Syndemics Theory to understand profiles of risk and resilience and their associations with substance use problems in a population at risk for adverse outcomes. African-American/Black and Hispanic heterosexual adults (N = 2,853) were recruited by respondent-driven sampling from an urban area with elevated poverty rates, and completed a structured assessment battery covering sociodemographics, syndemic factors (that is, multiple, co-occurring risk factors), and substance use. More than one-third of participants (36\\%) met criteria for either an alcohol or a drug problem in the past year. Latent class analysis identified profiles of risk and resilience, separately for women and men, which were associated with the probability of a substance use problem. Almost a third of women (27\\%) and 38\\% of men had lower risk profiles—patterns of resilience not apparent in other types of analyses. Profiles with more risk and fewer resilience factors were associated with an increased probability of substance use problems, but profiles with fewer risk and more resilience factors had rates of substance use problems that were very similar to the general adult population. Relative to the lowest risk profile, profiles with the most risk and fewest resilience factors were associated with increased odds of a substance use problem for both women [adjusted odds ratio (aOR) = 8.50; 95\\% CI: 3.85–18.74] and men (aOR = 11.68; 95\\% CI: 6.91–19.74). Addressing syndemic factors in substance use treatment and prevention may yield improved outcomes.},\n\turldate = {2018-04-25},\n\tjournal = {Frontiers in Public Health},\n\tauthor = {Cleland, Charles M. and Lanza, Stephanie T. and Vasilenko, Sara A. and Gwadz, Marya},\n\tmonth = sep,\n\tyear = {2017},\n\tpmid = {28936431},\n\tpmcid = {PMC5594078},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Gwadz, M.; Cleland, C. M; Perlman, D. C; Hagan, H.; Jenness, S. M; Leonard, N. R; Ritchie, A. S; and Kutnick, A.\n\n\n \n \n \n \n \n Public Health Benefit of Peer-Referral Strategies for Detecting Undiagnosed HIV Infection among High-Risk Heterosexuals in New York City.\n \n \n \n \n\n\n \n\n\n\n Journal of acquired immune deficiency syndromes (1999), 74(5): 499–507. April 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Public$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{gwadz_public_2017,\n\ttitle = {Public {Health} {Benefit} of {Peer}-{Referral} {Strategies} for {Detecting} {Undiagnosed} {HIV} {Infection} among {High}-{Risk} {Heterosexuals} in {New} {York} {City}},\n\tvolume = {74},\n\tissn = {1525-4135},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5341134/},\n\tdoi = {10.1097/QAI.0000000000001257},\n\tabstract = {Background\nIdentifying undiagnosed HIV infection is necessary for the elimination of HIV transmission in the United States. The present study evaluated the efficacy of three community-based approaches for uncovering undiagnosed HIV among heterosexuals at high-risk (HHR), who are mainly African American/Black and Hispanic. Heterosexuals comprise 24\\% of newly reported HIV infections in the U.S, but experience complex multi-level barriers to HIV testing.\n\nMethods\nWe recruited African American/Black and Hispanic HHR in a discrete urban area with both elevated HIV prevalence and poverty rates. Approaches tested were: 1) respondent-driven sampling (RDS) and confidential HIV testing in two sessions (n=3116); 2) RDS and anonymous HIV testing in one session (n=498); and 3) venue-based sampling (VBS) and HIV testing in a single session (n=403). The main outcome was newly diagnosed HIV infection.\n\nResults\nRDS with anonymous testing and one session reached HHR with less HIV testing experience and more risk factors than the other approaches. Further, RDS with anonymous (4.0\\%) and confidential (1.0\\%) testing yielded significantly higher rates of newly diagnosed HIV than VBS (0.3\\%).\n\nConclusion\nPeer-referral approaches were more efficacious than VBS for uncovering HHR with undiagnosed HIV, particularly a single-session/anonymous strategy, and have a vital role to play in efforts to eliminate HIV transmission.},\n\tnumber = {5},\n\turldate = {2018-04-25},\n\tjournal = {Journal of acquired immune deficiency syndromes (1999)},\n\tauthor = {Gwadz, Marya and Cleland, Charles M and Perlman, David C and Hagan, Holly and Jenness, Samuel M and Leonard, Noelle R and Ritchie, Amanda S and Kutnick, Alexandra},\n\tmonth = apr,\n\tyear = {2017},\n\tpmid = {28267698},\n\tpmcid = {PMC5341134},\n\tpages = {499--507},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Beaudry, IS; and Gile, KJ\n\n\n \n \n \n \n \n Inference for Respondent-Driven Sampling with Misclassification.\n \n \n \n \n\n\n \n\n\n\n The Annals of Applied Statistics, 11(4): 2111–2141. December 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Inference$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{beaudry_is_inference_2017,\n\ttitle = {Inference for {Respondent}-{Driven} {Sampling} with {Misclassification}},\n\tvolume = {11},\n\turl = {https://projecteuclid.org/download/pdfview_1/euclid.aoas/1514430279},\n\tabstract = {Mehta, SH},\n\tnumber = {4},\n\tjournal = {The Annals of Applied Statistics},\n\tauthor = {{Beaudry, IS} and {Gile, KJ}},\n\tmonth = dec,\n\tyear = {2017},\n\tpages = {2111--2141},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Walley, A. Y.; Cheng, D. M.; Quinn, E. K.; Blokhina, E.; Gnatienko, N.; Chaisson, C. E.; Krupitsky, E.; Coffin, P. O.; and Samet, J. H.\n\n\n \n \n \n \n \n Fatal and non-fatal overdose after narcology hospital discharge among Russians living with HIV/AIDS who inject drugs.\n \n \n \n \n\n\n \n\n\n\n The International Journal on Drug Policy, 39: 114–120. January 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Fatal$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{walley_fatal_2017,\n\ttitle = {Fatal and non-fatal overdose after narcology hospital discharge among {Russians} living with {HIV}/{AIDS} who inject drugs},\n\tvolume = {39},\n\tissn = {1873-4758},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5191979/},\n\tdoi = {10.1016/j.drugpo.2016.10.022},\n\tabstract = {OBJECTIVES: Among Russians living with HIV/AIDS who inject drugs, we examined the incidence of fatal and non-fatal overdoses following discharge from a narcology hospital and the associations with more advanced HIV infection.\nDESIGN: Prospective cohort study of data collected at baseline, 3 and 6 months from HIV-infected patients with a history of injection drug use who were not treated with anti-retroviral therapy. Participants were recruited between 2012-2014 from a narcology (addiction) hospital in St. Petersburg, Russia.\nMETHODS: Fatal overdose was determined based on contact reports to study staff in the year after discharge. Non-fatal overdose was self-reported at the 3- and 6-month assessments. The main independent variable for HIV severity was CD4 cell count at the baseline interview ({\\textless}200cells/mm(3)≥200cells/mm(3)). Secondary analyses assessed time since HIV diagnosis and treated with anti-retroviral treatment (ART) prior to enrolment as independent variables. We fit Cox proportional hazards models to assess whether HIV severity is associated with either fatal or non-fatal overdose.\nRESULTS: Among 349 narcology patients, 18 participants died from overdose within one year after discharge (8.7\\%, 95\\% CI 3.4-14.2 by Kaplan-Meier); an estimated 51\\% [95\\% CI 34-68\\%] reported at least one non-fatal overdose within 6 months of discharge. HIV severity, time since HIV diagnosis and ever ART were not significantly associated with either fatal or non-fatal overdose events.\nCONCLUSION: Fatal and non-fatal overdose are common among Russians living with HIV/AIDS who inject drugs after narcology hospital discharge. Overdose prevention interventions are urgently warranted among Russian narcology patients with HIV infection.},\n\tlanguage = {eng},\n\tjournal = {The International Journal on Drug Policy},\n\tauthor = {Walley, Alexander Y. and Cheng, Debbie M. and Quinn, Emily K. and Blokhina, Elena and Gnatienko, Natalia and Chaisson, Christine E. and Krupitsky, Evgeny and Coffin, Philip O. and Samet, Jeffrey H.},\n\tmonth = jan,\n\tyear = {2017},\n\tpmid = {27907848},\n\tpmcid = {PMC5191979},\n\tkeywords = {HIV, Injection drug use, Mortality, Overdose, Russia},\n\tpages = {114--120},\n}\n\n\n\n\n\n\n\n

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\n \n\n \n \n Lambdin, B. H.; Kral, A. H.; Comfort, M.; Lopez, A. M.; and Lorvick, J.\n\n\n \n \n \n \n \n Associations of criminal justice and substance use treatment involvement with HIV/HCV testing and the HIV treatment cascade among people who use drugs in Oakland, California.\n \n \n \n \n\n\n \n\n\n\n Addiction Science & Clinical Practice, 12(1): 13. June 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Associations$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{lambdin_associations_2017,\n\ttitle = {Associations of criminal justice and substance use treatment involvement with {HIV}/{HCV} testing and the {HIV} treatment cascade among people who use drugs in {Oakland}, {California}},\n\tvolume = {12},\n\tissn = {1940-0640},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5470222/},\n\tdoi = {10.1186/s13722-017-0078-9},\n\tabstract = {BACKGROUND: People who smoke crack cocaine and people who inject drugs are at-risk for criminal justice involvement as well as HIV and HCV infection. Compared to criminal justice involvement, substance use treatment (SUT) can be cost-effective in reducing drug use and its associated health and social costs. We conducted a cross-sectional study of people who smoke crack cocaine and people who inject drugs to examine the association between incarceration, community supervision and substance use treatment with HIV/HCV testing, components of the HIV treatment cascade, social and physical vulnerability and risk behavior.\nMETHODS: Targeted sampling methods were used to recruit people who smoke crack cocaine and people who inject drugs (N = 2072) in Oakland, California from 2011 to 2013. Poisson regression models were used to estimate adjusted prevalence ratios between study exposures and outcomes.\nRESULTS: The overall HIV prevalence was 3.3\\% (95\\% CI 2.6-4.1). People previously experiencing incarceration were 21\\% (p {\\textless} 0.001) and 32\\% (p = 0.001), respectively, more likely to report HIV and HCV testing; and were not more likely to report receiving HIV care or initiating ART. People previously experiencing community supervision were 17\\% (p = 0.001) and 15\\% (p = 0.009), respectively, more likely to report HIV and HCV testing; and were not more likely to report receiving HIV care or initiating ART. People with a history of SUT were 15\\% (p {\\textless} 0.001) and 23\\% (p {\\textless} 0.001), respectively, more likely to report receiving HIV and HCV testing, 67\\% (p = 0.016) more likely to report HIV care, and 92\\% (p = 0.012) more likely to report HIV treatment initiation. People previously experiencing incarceration or community supervision were also more likely to report homelessness, trouble meeting basic needs and risk behavior.\nCONCLUSIONS: People with a history of substance use treatment reported higher levels of HCV and HIV testing and greater access to HIV care and treatment among HIV-positive individuals. People with a history of incarceration or community supervision reported higher levels of HCV and HIV testing, but not greater access to HIV care or treatment among HIV-positive individuals., Substance use treatment programs that are integrated with other services for HIV and HCV will be critical to simultaneously address the underlying reasons drug-involved people engage in drug-related offenses and improve access to essential medical services.},\n\tlanguage = {eng},\n\tnumber = {1},\n\tjournal = {Addiction Science \\& Clinical Practice},\n\tauthor = {Lambdin, Barrot H. and Kral, Alex H. and Comfort, Megan and Lopez, Andrea M. and Lorvick, Jennifer},\n\tmonth = jun,\n\tyear = {2017},\n\tpmid = {28610602},\n\tpmcid = {PMC5470222},\n\tkeywords = {HIV, Hepatitis C, Implementation science, People who use drugs, Substance use treatment, criminal justice},\n\tpages = {13},\n}\n\n\n\n\n\n\n\n

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\n BACKGROUND: People who smoke crack cocaine and people who inject drugs are at-risk for criminal justice involvement as well as HIV and HCV infection. Compared to criminal justice involvement, substance use treatment (SUT) can be cost-effective in reducing drug use and its associated health and social costs. We conducted a cross-sectional study of people who smoke crack cocaine and people who inject drugs to examine the association between incarceration, community supervision and substance use treatment with HIV/HCV testing, components of the HIV treatment cascade, social and physical vulnerability and risk behavior. METHODS: Targeted sampling methods were used to recruit people who smoke crack cocaine and people who inject drugs (N = 2072) in Oakland, California from 2011 to 2013. Poisson regression models were used to estimate adjusted prevalence ratios between study exposures and outcomes. RESULTS: The overall HIV prevalence was 3.3% (95% CI 2.6-4.1). People previously experiencing incarceration were 21% (p \\textless 0.001) and 32% (p = 0.001), respectively, more likely to report HIV and HCV testing; and were not more likely to report receiving HIV care or initiating ART. People previously experiencing community supervision were 17% (p = 0.001) and 15% (p = 0.009), respectively, more likely to report HIV and HCV testing; and were not more likely to report receiving HIV care or initiating ART. People with a history of SUT were 15% (p \\textless 0.001) and 23% (p \\textless 0.001), respectively, more likely to report receiving HIV and HCV testing, 67% (p = 0.016) more likely to report HIV care, and 92% (p = 0.012) more likely to report HIV treatment initiation. People previously experiencing incarceration or community supervision were also more likely to report homelessness, trouble meeting basic needs and risk behavior. CONCLUSIONS: People with a history of substance use treatment reported higher levels of HCV and HIV testing and greater access to HIV care and treatment among HIV-positive individuals. People with a history of incarceration or community supervision reported higher levels of HCV and HIV testing, but not greater access to HIV care or treatment among HIV-positive individuals., Substance use treatment programs that are integrated with other services for HIV and HCV will be critical to simultaneously address the underlying reasons drug-involved people engage in drug-related offenses and improve access to essential medical services.\n

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\n \n\n \n \n Kral, A. H.; Lambdin, B. H.; Comfort, M.; Powers, C.; Cheng, H.; Lopez, A. M.; Murdoch, R. O.; Neilands, T. B.; and Lorvick, J.\n\n\n \n \n \n \n \n A Strengths-Based Case Management Intervention to Reduce HIV Viral Load Among People Who Use Drugs.\n \n \n \n \n\n\n \n\n\n\n AIDS and behavior. September 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{kral_strengths-based_2017,\n\ttitle = {A {Strengths}-{Based} {Case} {Management} {Intervention} to {Reduce} {HIV} {Viral} {Load} {Among} {People} {Who} {Use} {Drugs}},\n\tissn = {1573-3254},\n\turl = {https://link.springer.com/article/10.1007%2Fs10461-017-1903-6},\n\tdoi = {10.1007/s10461-017-1903-6},\n\tabstract = {Engaging highly marginalized HIV positive people in sustained medical care is vital for optimized health and prevention efforts. Prior studies have found that strengths-based case management helps link people who use drugs to HIV care. We conducted a pilot to assess whether a strengths-based case management intervention may help people who use injection drugs (PWID) or smoke crack cocaine (PWSC) achieve undetectable HIV viral load. PWID and PWSC were recruited in Oakland, California using targeted sampling methods and referral from jails and were tested for HIV. HIV positive participants not receiving HIV care (n = 19) were enrolled in a pilot strengths-based case management intervention and HIV positive participants already in HIV care (n = 29) were followed as comparison participants. The intervention was conducted by a social worker and an HIV physician. Special attention was given to coordinating care as participants cycled through jail and community settings. Surveys and HIV viral load tests were conducted quarterly for up to 11 visits. HIV viral load became undetectable for significantly more participants in the intervention than in the comparison group by their last follow-up (intervention participants: 32\\% at baseline and 74\\% at last follow-up; comparison participants: 45\\% at baseline and 34\\% at last follow-up; p = 0.008). In repeated measures analysis, PBO intervention participants had higher odds of achieving undetectable viral load over time than comparison participants (p = 0.033). Strengths-based case management may help this highly vulnerable group achieve undetectable HIV viral load over time.},\n\tlanguage = {eng},\n\tjournal = {AIDS and behavior},\n\tauthor = {Kral, Alex H. and Lambdin, Barrot H. and Comfort, Megan and Powers, Christina and Cheng, Helen and Lopez, Andrea M. and Murdoch, Robert O. and Neilands, Torsten B. and Lorvick, Jennifer},\n\tmonth = sep,\n\tyear = {2017},\n\tpmid = {28916898},\n\tkeywords = {Epidemiology, HIV, Intervention studies, Strengths-based case management, Viral load},\n}\n\n\n\n\n\n\n\n

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\n \n\n \n \n Lorvick, J.; Comfort, M.; Kral, A. H.; and Lambdin, B. H.\n\n\n \n \n \n \n \n Exploring Lifetime Accumulation of Criminal Justice Involvement and Associated Health and Social Outcomes in a Community-Based Sample of Women who Use Drugs.\n \n \n \n \n\n\n \n\n\n\n Journal of Urban Health: Bulletin of the New York Academy of Medicine. December 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Exploring$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{lorvick_exploring_2017,\n\ttitle = {Exploring {Lifetime} {Accumulation} of {Criminal} {Justice} {Involvement} and {Associated} {Health} and {Social} {Outcomes} in a {Community}-{Based} {Sample} of {Women} who {Use} {Drugs}},\n\tissn = {1468-2869},\n\turl = {https://link.springer.com/article/10.1007%2Fs11524-017-0204-8},\n\tdoi = {10.1007/s11524-017-0204-8},\n\tabstract = {Among people who use illegal drugs, engagement with the criminal justice (CJ) system often involves an ongoing, intermittent series of arrests, incarcerations, and periods of community supervision. The potential associations between the lifetime accumulation of CJ involvement and social and health outcomes is largely unexplored. In a cross-sectional sample of women who use crack, heroin, and/ or methamphetamine recruited from communities in Oakland, CA (N = 624), we developed an approach to characterize CJ accumulation. We used latent class analysis (LCA), a multivariate person-centered method that assumes an unobserved categorical variable that divides a population into a small number of mutually exclusive and exhaustive classes. Using observed measures of incarceration and community supervision as indicator variables, we developed a model of CJ accumulation that elucidates patterns of involvement as lived by the women in the sample. Based on model fit statistics, we selected a three-class model and labeled the classes "low," "medium," and "high." We then explored associations between the classes of CJ accumulation and health and health-related outcomes using logistic regression. The odds of homelessness (p for trend = 0.004), transience (p for trend = 0.017), and recent victimization (p for trend = 0.023) were higher among women in higher accumulation classes. Higher class of CJ accumulation was associated with higher odds of reporting unmet need for physical health care (p for trend {\\textless} 0.001) and mental health care (p for trend = 0.002). The odds of physical health conditions, such as hepatitis C infection (p for trend {\\textless} 0.001) and mental health conditions, such as depression (p for trend = 0.003), also increased with higher class of accumulation. While the findings described here are limited by the cross-sectional nature of the study, they suggest that CJ accumulation is a potentially meaningful concept for assessing associations between the CJ system and health-related issues.},\n\tlanguage = {eng},\n\tjournal = {Journal of Urban Health: Bulletin of the New York Academy of Medicine},\n\tauthor = {Lorvick, Jennifer and Comfort, Megan and Kral, Alex H. and Lambdin, Barrot H.},\n\tmonth = dec,\n\tyear = {2017},\n\tpmid = {29214435},\n\tkeywords = {Community supervision, Drug use, Incarceration, latent class analysis, women},\n}\n\n\n\n\n\n\n\n

\n\n\n

\n Among people who use illegal drugs, engagement with the criminal justice (CJ) system often involves an ongoing, intermittent series of arrests, incarcerations, and periods of community supervision. The potential associations between the lifetime accumulation of CJ involvement and social and health outcomes is largely unexplored. In a cross-sectional sample of women who use crack, heroin, and/ or methamphetamine recruited from communities in Oakland, CA (N = 624), we developed an approach to characterize CJ accumulation. We used latent class analysis (LCA), a multivariate person-centered method that assumes an unobserved categorical variable that divides a population into a small number of mutually exclusive and exhaustive classes. Using observed measures of incarceration and community supervision as indicator variables, we developed a model of CJ accumulation that elucidates patterns of involvement as lived by the women in the sample. Based on model fit statistics, we selected a three-class model and labeled the classes \"low,\" \"medium,\" and \"high.\" We then explored associations between the classes of CJ accumulation and health and health-related outcomes using logistic regression. The odds of homelessness (p for trend = 0.004), transience (p for trend = 0.017), and recent victimization (p for trend = 0.023) were higher among women in higher accumulation classes. Higher class of CJ accumulation was associated with higher odds of reporting unmet need for physical health care (p for trend \\textless 0.001) and mental health care (p for trend = 0.002). The odds of physical health conditions, such as hepatitis C infection (p for trend \\textless 0.001) and mental health conditions, such as depression (p for trend = 0.003), also increased with higher class of accumulation. While the findings described here are limited by the cross-sectional nature of the study, they suggest that CJ accumulation is a potentially meaningful concept for assessing associations between the CJ system and health-related issues.\n

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\n \n\n \n \n Solomon, S. S.; McFall, A. M.; Lucas, G. M.; Srikrishnan, A. K.; Kumar, M. S.; Anand, S.; Quinn, T. C.; Celentano, D. D.; and Mehta, S. H.\n\n\n \n \n \n \n \n Respondent-driven sampling for identification of HIV- and HCV-infected people who inject drugs and men who have sex with men in India: A cross-sectional, community-based analysis.\n \n \n \n \n\n\n \n\n\n\n PLoS medicine, 14(11): e1002460. November 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Respondent-driven$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{solomon_respondent-driven_2017,\n\ttitle = {Respondent-driven sampling for identification of {HIV}- and {HCV}-infected people who inject drugs and men who have sex with men in {India}: {A} cross-sectional, community-based analysis},\n\tvolume = {14},\n\tissn = {1549-1676},\n\tshorttitle = {Respondent-driven sampling for identification of {HIV}- and {HCV}-infected people who inject drugs and men who have sex with men in {India}},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5705124/},\n\tdoi = {10.1371/journal.pmed.1002460},\n\tabstract = {BACKGROUND: A major barrier to achieving ambitious targets for global control of HIV and hepatitis C virus (HCV) is low levels of awareness of infection among key populations such as men who have sex with men (MSM) and people who inject drugs (PWID). We explored the potential of a strategy routinely used for surveillance in these groups, respondent-driven sampling (RDS), to be used as an intervention to identify HIV- and HCV-infected PWID and MSM who are unaware of their status and those who are viremic across 26 Indian cities at various epidemic stages.\nMETHODS AND FINDINGS: Data were collected as part of the baseline assessment of an ongoing cluster-randomized trial. RDS was used to accrue participants at 27 sites (15 PWID sites and 12 MSM sites) selected to reflect varying stages of the HIV epidemic among MSM and PWID in India. A total of 56 seeds recruited a sample of 26,447 persons (approximately 1,000 participants per site) between October 1, 2012, and December 19, 2013. Across MSM sites (n = 11,997), the median age was 25 years and the median number of lifetime male partners was 8. Across PWID sites (n = 14,450), 92.4\\% were male, the median age was 30 years, and 87.5\\% reported injection in the prior 6 months. RDS identified 4,051 HIV-infected persons, of whom 2,325 (57.4\\%) were unaware of their HIV infection and 2,816 (69.5\\%) were HIV viremic. It also identified 5,777 HCV-infected persons, of whom 5,337 (92.4\\%) were unaware that they were infected with HCV and 4,728 (81.8\\%) were viremic. In the overall sample (both MSM and PWID), the prevalence of HIV-infected persons who were unaware of their status increased with sampling depth, from 7.9\\% in participants recruited in waves 1 through 5 to 12.8\\% among those recruited in waves 26 and above (p-value for trend {\\textless} 0.001). The overall detection rate of people unaware of their HIV infection was 0.5 persons per day, and the detection rate of HIV-infected persons with viremia (regardless of their awareness status) was 0.7 per day. The detection rate of HIV viremic individuals was positively associated with underlying HIV prevalence and the prevalence of HIV viremia (linear regression coefficient per 1-percentage-point increase in prevalence: 0.05 and 0.07, respectively). The median detection rate of PWID who were unaware of their HCV infection was 2.5 per day. The cost of identifying 1 unaware HIV-infected individual ranged from US\\$51 to US\\$2,072 across PWID sites and from US\\$189 to US\\$5,367 across MSM sites. The mean additional cost of identifying 1 unaware HCV-infected PWID was US\\$13 (site range: US\\$7-US\\$140). Limitations of the study include the exclusivity of study sites to India, lack of prior HIV/HCV diagnosis confirmation with clinic records, and lack of cost data from other case-finding approaches commonly used in India.\nCONCLUSIONS: In this study, RDS was able to rapidly identify at nominal cost a substantial number of unaware and viremic HIV-infected and HCV-infected individuals who were currently not being reached by existing programs and who were at high risk for transmission. Combining RDS (or other network-driven recruitment approaches) with strategies focused on linkage to care, particularly in high-burden settings, may be a viable option for achieving the 90-90-90 targets in key populations in resource-limited settings.},\n\tlanguage = {eng},\n\tnumber = {11},\n\tjournal = {PLoS medicine},\n\tauthor = {Solomon, Sunil S. and McFall, Allison M. and Lucas, Gregory M. and Srikrishnan, Aylur K. and Kumar, Muniratnam S. and Anand, Santhanam and Quinn, Thomas C. and Celentano, David D. and Mehta, Shruti H.},\n\tmonth = nov,\n\tyear = {2017},\n\tpmid = {29182638},\n\tpmcid = {PMC5705124},\n\tkeywords = {Adult, Community-Based Participatory Research, Community-Institutional Relations, Cross-Sectional Studies, HIV Infections, Hepacivirus, Hepatitis C, Homosexuality, Male, Humans, India, Male, Prevalence, Sexual Partners, Substance Abuse, Intravenous, Surveys and Questionnaires},\n\tpages = {e1002460},\n}\n\n\n\n\n\n\n\n

\n\n\n

\n BACKGROUND: A major barrier to achieving ambitious targets for global control of HIV and hepatitis C virus (HCV) is low levels of awareness of infection among key populations such as men who have sex with men (MSM) and people who inject drugs (PWID). We explored the potential of a strategy routinely used for surveillance in these groups, respondent-driven sampling (RDS), to be used as an intervention to identify HIV- and HCV-infected PWID and MSM who are unaware of their status and those who are viremic across 26 Indian cities at various epidemic stages. METHODS AND FINDINGS: Data were collected as part of the baseline assessment of an ongoing cluster-randomized trial. RDS was used to accrue participants at 27 sites (15 PWID sites and 12 MSM sites) selected to reflect varying stages of the HIV epidemic among MSM and PWID in India. A total of 56 seeds recruited a sample of 26,447 persons (approximately 1,000 participants per site) between October 1, 2012, and December 19, 2013. Across MSM sites (n = 11,997), the median age was 25 years and the median number of lifetime male partners was 8. Across PWID sites (n = 14,450), 92.4% were male, the median age was 30 years, and 87.5% reported injection in the prior 6 months. RDS identified 4,051 HIV-infected persons, of whom 2,325 (57.4%) were unaware of their HIV infection and 2,816 (69.5%) were HIV viremic. It also identified 5,777 HCV-infected persons, of whom 5,337 (92.4%) were unaware that they were infected with HCV and 4,728 (81.8%) were viremic. In the overall sample (both MSM and PWID), the prevalence of HIV-infected persons who were unaware of their status increased with sampling depth, from 7.9% in participants recruited in waves 1 through 5 to 12.8% among those recruited in waves 26 and above (p-value for trend \\textless 0.001). The overall detection rate of people unaware of their HIV infection was 0.5 persons per day, and the detection rate of HIV-infected persons with viremia (regardless of their awareness status) was 0.7 per day. The detection rate of HIV viremic individuals was positively associated with underlying HIV prevalence and the prevalence of HIV viremia (linear regression coefficient per 1-percentage-point increase in prevalence: 0.05 and 0.07, respectively). The median detection rate of PWID who were unaware of their HCV infection was 2.5 per day. The cost of identifying 1 unaware HIV-infected individual ranged from US$51 to US$2,072 across PWID sites and from US$189 to US$5,367 across MSM sites. The mean additional cost of identifying 1 unaware HCV-infected PWID was US$13 (site range: US$7-US$140). Limitations of the study include the exclusivity of study sites to India, lack of prior HIV/HCV diagnosis confirmation with clinic records, and lack of cost data from other case-finding approaches commonly used in India. CONCLUSIONS: In this study, RDS was able to rapidly identify at nominal cost a substantial number of unaware and viremic HIV-infected and HCV-infected individuals who were currently not being reached by existing programs and who were at high risk for transmission. Combining RDS (or other network-driven recruitment approaches) with strategies focused on linkage to care, particularly in high-burden settings, may be a viable option for achieving the 90-90-90 targets in key populations in resource-limited settings.\n

\n\n\n

\n \n\n \n \n Idrisov, B.; Lunze, K.; Cheng, D. M.; Blokhina, E.; Gnatienko, N.; Quinn, E.; Bridden, C.; Walley, A. Y.; Bryant, K. J.; Lioznov, D.; Krupitsky, E.; and Samet, J. H.\n\n\n \n \n \n \n \n Role of substance use in HIV care cascade outcomes among people who inject drugs in Russia.\n \n \n \n \n\n\n \n\n\n\n Addiction Science & Clinical Practice, 12(1): 30. December 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Role$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{idrisov_role_2017,\n\ttitle = {Role of substance use in {HIV} care cascade outcomes among people who inject drugs in {Russia}},\n\tvolume = {12},\n\tissn = {1940-0640},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5713116/},\n\tdoi = {10.1186/s13722-017-0098-5},\n\tabstract = {BACKGROUND: Engaging people who drink alcohol or inject drugs in HIV care can be challenging, particularly in Eastern Europe. Healthcare facilities in Russia are organized by specialty; therefore linking patients from addiction care to HIV hospitals has been difficult. The HIV care cascade outlines stages of HIV care (e.g., linkage to care, prescribed antiretroviral therapy [ART], and achieving HIV viral suppression). We hypothesized that unhealthy alcohol use, injection drug use, and opioid craving are associated with unfavorable HIV care cascade outcomes.\nMETHODS: We analyzed data from a cohort (n = 249) of HIV-positive Russians who have been in addiction hospital treatment in the past year and had a lifetime history of injection drug use (IDU). We evaluated the association between unhealthy alcohol use (AUDIT score {\\textgreater} 7 [both hazardous drinking and dependence]), past-month injection drug use (IDU), and opioid craving (visual analogue scale from 1 to 100) with HIV care cascade outcomes. The primary outcome was linkage to HIV care within 12 months. Other outcomes were prescription of ART (secondary) and achievement of undetectable HIV viral load (HVL {\\textless} 500 copies/mL) within 12 months (exploratory); the latter was analyzed on a subset in which HVL was measured (n = 48). We assessed outcomes via medical record review (linkage, ART) and serum tests (HVL). To examine the primary outcome, we used multiple logistic regression models controlling for potential confounders.\nRESULTS: Among 249 study participants, unhealthy alcohol use (n = 148 [59\\%]) and past-month IDU (n = 130 [52\\%]) were common. The mean opioid craving score was 49 (SD: 38). We were unable to detect significant associations between the independent variables (i.e., unhealthy alcohol use, IDU and opioid craving) and any HIV care cascade outcomes in unadjusted and adjusted analyses.\nCONCLUSION: In this cohort of HIV-positive Russians with a history of IDU, individual substance use factors were not significantly associated with achieving HIV care cascade milestones (i.e., linkage to HIV care; prescription for ART; or suppressed viral load). Given no detection of an association of cascade outcomes with recent unhealthy use of alcohol or injection drugs in this cohort, examining systemic factors to understand determinants of HIV care engagement for people with drug use would be important.},\n\tlanguage = {eng},\n\tnumber = {1},\n\tjournal = {Addiction Science \\& Clinical Practice},\n\tauthor = {Idrisov, Bulat and Lunze, Karsten and Cheng, Debbie M. and Blokhina, Elena and Gnatienko, Natalia and Quinn, Emily and Bridden, Carly and Walley, Alexander Y. and Bryant, Kendall J. and Lioznov, Dmitry and Krupitsky, Evgeny and Samet, Jeffrey H.},\n\tmonth = dec,\n\tyear = {2017},\n\tpmid = {29198185},\n\tpmcid = {PMC5713116},\n\tkeywords = {ART, HIV care cascade, Injection drug use, Opioid craving, Russia, Suppressed viral load, Unhealthy alcohol use, linkage to care},\n\tpages = {30},\n}\n\n\n\n\n\n\n\n

\n\n\n

\n BACKGROUND: Engaging people who drink alcohol or inject drugs in HIV care can be challenging, particularly in Eastern Europe. Healthcare facilities in Russia are organized by specialty; therefore linking patients from addiction care to HIV hospitals has been difficult. The HIV care cascade outlines stages of HIV care (e.g., linkage to care, prescribed antiretroviral therapy [ART], and achieving HIV viral suppression). We hypothesized that unhealthy alcohol use, injection drug use, and opioid craving are associated with unfavorable HIV care cascade outcomes. METHODS: We analyzed data from a cohort (n = 249) of HIV-positive Russians who have been in addiction hospital treatment in the past year and had a lifetime history of injection drug use (IDU). We evaluated the association between unhealthy alcohol use (AUDIT score \\textgreater 7 [both hazardous drinking and dependence]), past-month injection drug use (IDU), and opioid craving (visual analogue scale from 1 to 100) with HIV care cascade outcomes. The primary outcome was linkage to HIV care within 12 months. Other outcomes were prescription of ART (secondary) and achievement of undetectable HIV viral load (HVL \\textless 500 copies/mL) within 12 months (exploratory); the latter was analyzed on a subset in which HVL was measured (n = 48). We assessed outcomes via medical record review (linkage, ART) and serum tests (HVL). To examine the primary outcome, we used multiple logistic regression models controlling for potential confounders. RESULTS: Among 249 study participants, unhealthy alcohol use (n = 148 [59%]) and past-month IDU (n = 130 [52%]) were common. The mean opioid craving score was 49 (SD: 38). We were unable to detect significant associations between the independent variables (i.e., unhealthy alcohol use, IDU and opioid craving) and any HIV care cascade outcomes in unadjusted and adjusted analyses. CONCLUSION: In this cohort of HIV-positive Russians with a history of IDU, individual substance use factors were not significantly associated with achieving HIV care cascade milestones (i.e., linkage to HIV care; prescription for ART; or suppressed viral load). Given no detection of an association of cascade outcomes with recent unhealthy use of alcohol or injection drugs in this cohort, examining systemic factors to understand determinants of HIV care engagement for people with drug use would be important.\n

\n\n\n

\n \n\n \n \n West, B. S.; Cheng, D. M.; Toussova, O.; Blokhina, E.; Gnatienko, N.; Liu, K.; Samet, J. H.; and Raj, A.\n\n\n \n \n \n \n \n Contraceptive Use Among HIV-Infected Females with History of Injection Drug Use in St. Petersburg, Russia.\n \n \n \n \n\n\n \n\n\n\n AIDS and behavior. November 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Contraceptive$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{west_contraceptive_2017,\n\ttitle = {Contraceptive {Use} {Among} {HIV}-{Infected} {Females} with {History} of {Injection} {Drug} {Use} in {St}. {Petersburg}, {Russia}},\n\tissn = {1573-3254},\n\turl = {https://link.springer.com/article/10.1007%2Fs10461-017-1990-4},\n\tdoi = {10.1007/s10461-017-1990-4},\n\tabstract = {Limited research examines family planning for HIV-infected women with a history of injection drug use. We describe modern contraceptive use and its association with heavy drinking and recent injection for HIV-infected females in St. Petersburg, Russia (N = 49): 22.4\\% (n = 11) used traditional methods and 30.6\\% (n = 15) reported modern contraceptive use, which consisted primarily of condoms (26.5\\%, n = 13). Over 63\\% (n = 31) had an abortion. Observed associations for heavy alcohol use (AOR = 2.36, CI = 0.53, 12.41) and recent injection drug use (AOR = 2.88, CI = 0.60, 16.92) were clinically notable, but not statistically significant. Prioritizing family planning for HIV-infected women with a history of substance use is urgently needed.},\n\tlanguage = {eng},\n\tjournal = {AIDS and behavior},\n\tauthor = {West, Brooke S. and Cheng, Debbie M. and Toussova, Olga and Blokhina, Elena and Gnatienko, Natalia and Liu, Kan and Samet, Jeffrey H. and Raj, Anita},\n\tmonth = nov,\n\tyear = {2017},\n\tpmid = {29170946},\n\tkeywords = {Females, HIV-infected, Injection drug use, Modern contraceptive use, Russia},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Wooditch, A.; Mbaba, M.; Kiss, M.; Lawson, W.; Taxman, F.; and Altice, F. L.\n\n\n \n \n \n \n \n Housing Experiences among Opioid-Dependent, Criminal Justice-Involved Individuals in Washington, D.C.\n \n \n \n \n\n\n \n\n\n\n Journal of Urban Health,1–10. May 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Housing$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{wooditch_housing_2017,\n\ttitle = {Housing {Experiences} among {Opioid}-{Dependent}, {Criminal} {Justice}-{Involved} {Individuals} in {Washington}, {D}.{C}.},\n\tissn = {1099-3460, 1468-2869},\n\turl = {https://link.springer.com/article/10.1007/s11524-017-0156-z},\n\tdoi = {10.1007/s11524-017-0156-z},\n\tabstract = {Residential mobility and type of housing contributes to an individual’s likelihood and frequency of drug/alcohol use and committing criminal offenses. Little research has focused simultaneously on the influence of housing status on the use of drugs and criminal behavior. The present study examines how residential mobility (transitions in housing) and recent housing stability (prior 30 days) correlates with self-reported criminal activity and drug/alcohol use among a sample of 504 addicted, treatment-seeking opioid users with a history of criminal justice involvement. Findings suggest that those with a greater number of housing transitions were considerably less likely to self-report criminal activity, and criminal involvement was highest among those who were chronically homeless. Residential mobility was unassociated with days of drug and alcohol use; however, residing in regulated housing (halfway houses and homeless shelters) was associated with a decreased frequency of substance use. The finding that residing at sober-living housing facilities with regulations governing behavior (regulated housing) was associated with a lower likelihood of illicit substance use may suggest that regulated housing settings may influence behavior. Further research in this area should explore how social networks and other related variables moderate the effects of housing type and mobility on crime and substance use.},\n\tlanguage = {en},\n\turldate = {2017-09-26},\n\tjournal = {Journal of Urban Health},\n\tauthor = {Wooditch, Alese and Mbaba, Mary and Kiss, Marissa and Lawson, William and Taxman, Faye and Altice, Frederick L.},\n\tmonth = may,\n\tyear = {2017},\n\tpages = {1--10},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Kutnick, A. H.; Gwadz, M. V.; Cleland, C. M.; Leonard, N. R.; Freeman, R.; Ritchie, A. S.; McCright-Gill, T.; Ha, K.; and Martinez, B. Y.\n\n\n \n \n \n \n \n It’s a Process: Reactions to HIV Diagnosis and Engagement in HIV Care among High-Risk Heterosexuals.\n \n \n \n \n\n\n \n\n\n\n Frontiers in Public Health, 5. May 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"It’s$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{kutnick_its_2017,\n\ttitle = {It’s a {Process}: {Reactions} to {HIV} {Diagnosis} and {Engagement} in {HIV} {Care} among {High}-{Risk} {Heterosexuals}},\n\tvolume = {5},\n\tissn = {2296-2565},\n\tshorttitle = {It’s a {Process}},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5423945/},\n\tdoi = {10.3389/fpubh.2017.00100},\n\tabstract = {After HIV diagnosis, heterosexuals in high-poverty urban areas evidence delays in linkage to care and antiretroviral therapy initiation compared to other groups. Yet barriers to/facilitators of HIV care among these high-risk heterosexuals are understudied. Under the theory of triadic influence, putative barriers to HIV care engagement include individual/attitudinal-level (e.g., fear, medical distrust), social-level (e.g., stigma), and structural-level influences (e.g., poor access). Participants were African-American/Black and Hispanic adults found newly diagnosed with HIV (N = 25) as part of a community-based HIV testing study with heterosexuals in a high-poverty, high-HIV-incidence urban area. A sequential explanatory mixed-methods design was used. We described linkage to HIV care and clinical outcomes [CD4 counts, viral load (VL) levels] over 1 year, and then addressed qualitative research questions about the experience of receiving a new HIV diagnosis, its effects on timely engagement in HIV care, and other barriers and facilitators. Participants were assessed five times, receiving a structured interview battery, laboratory tests, data extraction from the medical record, a post-test counseling session, and in-person/phone contacts to foster linkage to care. Participants were randomly selected for qualitative interviews (N = 15/25) that were recorded and transcribed, then analyzed using systematic content analysis. Participants were 50 years old, on average (SD = 7.2 years), mostly male (80\\%), primarily African-American/Black (88\\%), and low socioeconomic status. At the first follow-up, rates of engagement in care were high (78\\%), but viral suppression was modest (39\\%). Rates improved by the final follow-up (96\\% engaged, 62\\% virally suppressed). Two-thirds (69\\%) were adequately retained in care over 1 year. Qualitative results revealed multi-faceted responses to receiving an HIV diagnosis. Problems accepting and internalizing one’s HIV status were common. Reaching acceptance of one’s HIV-infected status was frequently a protracted and circuitous process, but acceptance is vital for engagement in HIV care. Fear of stigma and loss of important relationships were potent barriers to acceptance. Thus, partially as a result of difficulties accepting HIV status, delays in achieving an undetectable VL are common in this population, with serious potential negative consequences for individual and public health. Interventions to foster acceptance of HIV status are needed.},\n\tjournal = {Frontiers in Public Health},\n\tauthor = {Kutnick, Alexandra H. and Gwadz, Marya Viorst and Cleland, Charles M. and Leonard, Noelle R. and Freeman, Robert and Ritchie, Amanda S. and McCright-Gill, Talaya and Ha, Kathy and Martinez, Belkis Y.},\n\tmonth = may,\n\tyear = {2017},\n\tpmid = {28540287},\n\tpmcid = {PMC5423945},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n After HIV diagnosis, heterosexuals in high-poverty urban areas evidence delays in linkage to care and antiretroviral therapy initiation compared to other groups. Yet barriers to/facilitators of HIV care among these high-risk heterosexuals are understudied. Under the theory of triadic influence, putative barriers to HIV care engagement include individual/attitudinal-level (e.g., fear, medical distrust), social-level (e.g., stigma), and structural-level influences (e.g., poor access). Participants were African-American/Black and Hispanic adults found newly diagnosed with HIV (N = 25) as part of a community-based HIV testing study with heterosexuals in a high-poverty, high-HIV-incidence urban area. A sequential explanatory mixed-methods design was used. We described linkage to HIV care and clinical outcomes [CD4 counts, viral load (VL) levels] over 1 year, and then addressed qualitative research questions about the experience of receiving a new HIV diagnosis, its effects on timely engagement in HIV care, and other barriers and facilitators. Participants were assessed five times, receiving a structured interview battery, laboratory tests, data extraction from the medical record, a post-test counseling session, and in-person/phone contacts to foster linkage to care. Participants were randomly selected for qualitative interviews (N = 15/25) that were recorded and transcribed, then analyzed using systematic content analysis. Participants were 50 years old, on average (SD = 7.2 years), mostly male (80%), primarily African-American/Black (88%), and low socioeconomic status. At the first follow-up, rates of engagement in care were high (78%), but viral suppression was modest (39%). Rates improved by the final follow-up (96% engaged, 62% virally suppressed). Two-thirds (69%) were adequately retained in care over 1 year. Qualitative results revealed multi-faceted responses to receiving an HIV diagnosis. Problems accepting and internalizing one’s HIV status were common. Reaching acceptance of one’s HIV-infected status was frequently a protracted and circuitous process, but acceptance is vital for engagement in HIV care. Fear of stigma and loss of important relationships were potent barriers to acceptance. Thus, partially as a result of difficulties accepting HIV status, delays in achieving an undetectable VL are common in this population, with serious potential negative consequences for individual and public health. Interventions to foster acceptance of HIV status are needed.\n

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\n \n\n \n \n Chandler, R.; Gordon, M. S.; Kruszka, B.; Strand, L. N.; Altice, F. L.; Beckwith, C. G.; Biggs, M. L.; Cunningham, W.; Chris Delaney, J. A.; Flynn, P. M.; Golin, C. E.; Knight, K.; Kral, A. H.; Kuo, I.; Lorvick, J.; Nance, R. M.; Ouellet, L. J.; Rich, J. D.; Sacks, S.; Seal, D.; Spaulding, A.; Springer, S. A.; Taxman, F.; Wohl, D.; Young, J. D.; Young, R.; and Crane, H. M.\n\n\n \n \n \n \n \n Cohort profile: seek, test, treat and retain United States criminal justice cohort.\n \n \n \n \n\n\n \n\n\n\n Substance Abuse Treatment, Prevention, and Policy, 12(1): 24. May 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Cohort$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{chandler_cohort_2017,\n\ttitle = {Cohort profile: seek, test, treat and retain {United} {States} criminal justice cohort},\n\tvolume = {12},\n\tissn = {1747-597X},\n\tshorttitle = {Cohort profile},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5433052/},\n\tdoi = {10.1186/s13011-017-0107-4},\n\tabstract = {BACKGROUND: The STTR treatment cascade provides a framework for research aimed at improving the delivery of services, care and outcomes of PLWH. The development of effective approaches to increase HIV diagnoses and engage PLWH in subsequent steps of the treatment cascade could lead to earlier and sustained ART treatment resulting in viral suppression. There is an unmet need for research applying the treatment cascade to improve outcomes for those with criminal justice involvement.\nMETHODS: The Seek, Test, Treat, and Retain (STTR) criminal justice (CJ) cohort combines data from 11 studies across the HIV treatment cascade that focused on persons involved in the criminal justice system, often but not exclusively for reasons related to substance use. The studies were conducted in a variety of CJ settings and collected information across 11 pre-selected domains: demographic characteristics, CJ involvement, HIV risk behaviors, HIV and/or Hepatitis C infections, laboratory measures of CD4 T-cell count (CD4) and HIV RNA viral load (VL), mental illness, health related quality of life (QoL), socioeconomic status, health care access, substance use, and social support.\nRESULTS: The STTR CJ cohort includes data on 11,070 individuals with and without HIV infection who range in age from 18 to 77 years, with a median age at baseline of 37 years. The cohort reflects racial, ethnic and gender distributions in the U.S. CJ system, and 64\\% of participants are African-American, 12\\% are Hispanic and 83\\% are men. Cohort members reported a wide range of HIV risk behaviors including history of injection drug use and, among those who reported on pre-incarceration sexual behaviors, the prevalence of unprotected sexual intercourse ranged across studies from 4\\% to 79\\%. Across all studies, 53\\% percent of the STTR CJ cohort reported recent polysubstance use.\nCONCLUSIONS: The STTR CJ cohort is comprised of participants from a wide range of CJ settings including jail, prison, and community supervision who report considerable diversity in their characteristics and behavioral practices. We have developed harmonized measures, where feasible, to improve the integration of these studies together to answer questions that cannot otherwise be addressed.},\n\tlanguage = {eng},\n\tnumber = {1},\n\tjournal = {Substance Abuse Treatment, Prevention, and Policy},\n\tauthor = {Chandler, Redonna and Gordon, Michael S. and Kruszka, Bridget and Strand, Lauren N. and Altice, Frederick L. and Beckwith, Curt G. and Biggs, Mary L. and Cunningham, William and Chris Delaney, J. A. and Flynn, Patrick M. and Golin, Carol E. and Knight, Kevin and Kral, Alex H. and Kuo, Irene and Lorvick, Jennifer and Nance, Robin M. and Ouellet, Lawrence J. and Rich, Josiah D. and Sacks, Stanley and Seal, David and Spaulding, Anne and Springer, Sandra A. and Taxman, Faye and Wohl, David and Young, Jeremy D. and Young, Rebekah and Crane, Heidi M.},\n\tmonth = may,\n\tyear = {2017},\n\tpmid = {28511680},\n\tpmcid = {PMC5433052},\n\tkeywords = {Data harmonization., HIV, STTR Core, criminal justice},\n\tpages = {24},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

\n\n\n

\n BACKGROUND: The STTR treatment cascade provides a framework for research aimed at improving the delivery of services, care and outcomes of PLWH. The development of effective approaches to increase HIV diagnoses and engage PLWH in subsequent steps of the treatment cascade could lead to earlier and sustained ART treatment resulting in viral suppression. There is an unmet need for research applying the treatment cascade to improve outcomes for those with criminal justice involvement. METHODS: The Seek, Test, Treat, and Retain (STTR) criminal justice (CJ) cohort combines data from 11 studies across the HIV treatment cascade that focused on persons involved in the criminal justice system, often but not exclusively for reasons related to substance use. The studies were conducted in a variety of CJ settings and collected information across 11 pre-selected domains: demographic characteristics, CJ involvement, HIV risk behaviors, HIV and/or Hepatitis C infections, laboratory measures of CD4 T-cell count (CD4) and HIV RNA viral load (VL), mental illness, health related quality of life (QoL), socioeconomic status, health care access, substance use, and social support. RESULTS: The STTR CJ cohort includes data on 11,070 individuals with and without HIV infection who range in age from 18 to 77 years, with a median age at baseline of 37 years. The cohort reflects racial, ethnic and gender distributions in the U.S. CJ system, and 64% of participants are African-American, 12% are Hispanic and 83% are men. Cohort members reported a wide range of HIV risk behaviors including history of injection drug use and, among those who reported on pre-incarceration sexual behaviors, the prevalence of unprotected sexual intercourse ranged across studies from 4% to 79%. Across all studies, 53% percent of the STTR CJ cohort reported recent polysubstance use. CONCLUSIONS: The STTR CJ cohort is comprised of participants from a wide range of CJ settings including jail, prison, and community supervision who report considerable diversity in their characteristics and behavioral practices. We have developed harmonized measures, where feasible, to improve the integration of these studies together to answer questions that cannot otherwise be addressed.\n

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\n \n\n \n \n Powers, C.; Comfort, M.; Lopez, A. M.; Kral, A. H.; Murdoch, O.; and Lorvick, J.\n\n\n \n \n \n \n \n Addressing Structural Barriers to HIV Care among Triply Diagnosed Adults: Project Bridge Oakland.\n \n \n \n \n\n\n \n\n\n\n Health & Social Work,1–9. March 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Addressing$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{powers_addressing_2017,\n\ttitle = {Addressing {Structural} {Barriers} to {HIV} {Care} among {Triply} {Diagnosed} {Adults}: {Project} {Bridge} {Oakland}},\n\tshorttitle = {Addressing {Structural} {Barriers} to {HIV} {Care} among {Triply} {Diagnosed} {Adults}},\n\turl = {https://academic.oup.com/hsw/article/doi/10.1093/hsw/hlx013/3069322/Addressing-Structural-Barriers-to-HIV-Care-among},\n\tdoi = {10.1093/hsw/hlx013},\n\turldate = {2017-04-05},\n\tjournal = {Health \\& Social Work},\n\tauthor = {Powers, Christina and Comfort, Megan and Lopez, Andrea M. and Kral, Alex H. and Murdoch, Owen and Lorvick, Jennifer},\n\tmonth = mar,\n\tyear = {2017},\n\tpages = {1--9},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Sabri, B.; McFall, A. M.; Solomon, S. S.; Srikrishnan, A. K.; Vasudevan, C. K.; Anand, S.; Celentano, D. D.; Mehta, S. H.; Kumar, S.; and Lucas, G. M.\n\n\n \n \n \n \n \n Gender Differences in Factors Related to HIV Risk Behaviors among People Who Inject Drugs in North-East India.\n \n \n \n \n\n\n \n\n\n\n PLoS ONE, 12(1). January 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Gender$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{sabri_gender_2017,\n\ttitle = {Gender {Differences} in {Factors} {Related} to {HIV} {Risk} {Behaviors} among {People} {Who} {Inject} {Drugs} in {North}-{East} {India}},\n\tvolume = {12},\n\tissn = {1932-6203},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5242464/},\n\tdoi = {10.1371/journal.pone.0169482},\n\tabstract = {People who inject drugs (PWID) in India are at high risk for HIV, with women being at elevated risk. Using a socio-ecological framework, this study assessed whether factors associated with HIV transmission risk behaviors differed across men and women PWID. Data for this cross-sectional study were collected from 6449 PWID in 7 cities in Northeast India. Men (n = 5653) and women (n = 796) PWID were recruited using respondent-driven sampling (RDS). We assessed sex differences in two recent HIV transmission risk behaviors: multiple sex partners and needle/syringe sharing. We used multi-level logistic regression models, which incorporated sampling weights and random intercepts for city, to assess factors associated with these HIV risks, separately among men and women. The prevalence of HIV was significantly higher among women than men (53\\% vs 18.4\\%, p{\\textless}0.01). Nearly 13\\% of men and 8\\% of women (p = .30) had multiple partners. Employment in men and relationship status and stigma in women were significantly associated with multiple partners. Approximately 25\\% of men and 19\\% of women engaged in needle sharing (p = .16). Younger age in women and depression symptoms in men were significantly associated with increased risk for sharing needles. We found that sexual and drug related risk behaviors were common among PWID in Northeast India, and there were differences between men and women in the socio-ecologic correlates of these behaviors. Contextually-integrated and gender-specific HIV prevention and intervention efforts are needed that consider factors at individual, interpersonal- and community-levels that uniquely impact HIV risks among PWID.},\n\tnumber = {1},\n\turldate = {2017-04-05},\n\tjournal = {PLoS ONE},\n\tauthor = {Sabri, Bushra and McFall, Allison M. and Solomon, Sunil S. and Srikrishnan, Aylur K. and Vasudevan, Canjeevaram K. and Anand, Santhanam and Celentano, David D. and Mehta, Shruti H. and Kumar, Suresh and Lucas, Gregory M.},\n\tmonth = jan,\n\tyear = {2017},\n\tpmid = {28099458},\n\tpmcid = {PMC5242464},\n}\n\n\n\n\n\n\n\n

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\n \n\n \n \n Beckwith, C.; Castonguay, B. U.; Trezza, C.; Bazerman, L.; Patrick, R.; Cates, A.; Olsen, H.; Kurth, A.; Liu, T.; Peterson, J.; and Kuo, I.\n\n\n \n \n \n \n \n Gender Differences in HIV Care among Criminal Justice-Involved Persons: Baseline Data from the CARE+ Corrections Study.\n \n \n \n \n\n\n \n\n\n\n PloS One, 12(1): e0169078. January 2017.\n \n\n\n\n
\n\n\n\n \n \n $\"Gender$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{beckwith_gender_2017,\n\ttitle = {Gender {Differences} in {HIV} {Care} among {Criminal} {Justice}-{Involved} {Persons}: {Baseline} {Data} from the {CARE}+ {Corrections} {Study}},\n\tvolume = {12},\n\tissn = {1932-6203},\n\tshorttitle = {Gender {Differences} in {HIV} {Care} among {Criminal} {Justice}-{Involved} {Persons}},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5231337/},\n\tdoi = {10.1371/journal.pone.0169078},\n\tabstract = {BACKGROUND: HIV-infected individuals recently released from incarceration have suboptimal linkage and engagement in community HIV care. We conducted a study to evaluate an information and communication technology intervention to increase linkage to community care among HIV-infected persons recently involved in the criminal justice (CJ) system. Baseline characteristics including risk behaviors and HIV care indicators are reported and stratified by gender.\nMETHODS: We recruited HIV-infected individuals in the District of Columbia jail and persons with a recent history of incarceration through community and street outreach. Participants completed a baseline computer-assisted personal interview regarding HIV care and antiretroviral treatment (ART) adherence, substance use, and sexual behaviors. CD4 and HIV plasma viral load testing were performed at baseline or obtained through medical records. Data were analyzed for the sample overall and stratified by gender.\nRESULTS: Of 110 individuals, 70\\% were community-enrolled, mean age was 40 (SD = 10.5), 85\\% were Black, and 58\\% were male, 24\\% female, and 18\\% transgender women. Nearly half (47\\%) had condomless sex in the three months prior to incarceration. Although drug dependence and hazardous alcohol use were highly prevalent overall, transgender women were more likely to have participated in drug treatment than men and women (90\\%, 61\\%, and 50\\% respectively; p = 0.01). Prior to their most recent incarceration, 80\\% had an HIV provider and 91\\% had ever taken ART. Among those, only 51\\% reported ≥90\\% ART adherence. Fewer women (67\\%) had received HIV medications during their last incarceration compared to men (96\\%) and transgender women (95\\%; p = 0.001). Although neither was statistically significant, transgender women and men had higher proportions of baseline HIV viral suppression compared to women (80\\%, 69\\%, and 48.0\\% respectively, p{\\textgreater}0.05); a higher proportion of women had a CD4 count ≤200 compared to men and transgender women (17\\%, 8\\% and 5\\% respectively; p{\\textgreater}0.05).\nCONCLUSIONS: In this study, HIV-infected persons with recent incarceration in Washington, DC reported important risk factors and co-morbidities, yet the majority had access to HIV care and ART prior to, during, and after incarceration. Self-reported ART adherence was sub-optimal, and while there were not statistically significant differences, CJ-involved women appeared to be at greatest risk of poor HIV outcomes.\nTRIAL REGISTRATION: Registered on ClinicalTrials.gov on 10/16/2012. Reference number: NCT01721226.},\n\tlanguage = {eng},\n\tnumber = {1},\n\tjournal = {PloS One},\n\tauthor = {Beckwith, Curt and Castonguay, Breana Uhrig and Trezza, Claudia and Bazerman, Lauri and Patrick, Rudy and Cates, Alice and Olsen, Halli and Kurth, Ann and Liu, Tao and Peterson, James and Kuo, Irene},\n\tmonth = jan,\n\tyear = {2017},\n\tpmid = {28081178},\n\tpages = {e0169078},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n BACKGROUND: HIV-infected individuals recently released from incarceration have suboptimal linkage and engagement in community HIV care. We conducted a study to evaluate an information and communication technology intervention to increase linkage to community care among HIV-infected persons recently involved in the criminal justice (CJ) system. Baseline characteristics including risk behaviors and HIV care indicators are reported and stratified by gender. METHODS: We recruited HIV-infected individuals in the District of Columbia jail and persons with a recent history of incarceration through community and street outreach. Participants completed a baseline computer-assisted personal interview regarding HIV care and antiretroviral treatment (ART) adherence, substance use, and sexual behaviors. CD4 and HIV plasma viral load testing were performed at baseline or obtained through medical records. Data were analyzed for the sample overall and stratified by gender. RESULTS: Of 110 individuals, 70% were community-enrolled, mean age was 40 (SD = 10.5), 85% were Black, and 58% were male, 24% female, and 18% transgender women. Nearly half (47%) had condomless sex in the three months prior to incarceration. Although drug dependence and hazardous alcohol use were highly prevalent overall, transgender women were more likely to have participated in drug treatment than men and women (90%, 61%, and 50% respectively; p = 0.01). Prior to their most recent incarceration, 80% had an HIV provider and 91% had ever taken ART. Among those, only 51% reported ≥90% ART adherence. Fewer women (67%) had received HIV medications during their last incarceration compared to men (96%) and transgender women (95%; p = 0.001). Although neither was statistically significant, transgender women and men had higher proportions of baseline HIV viral suppression compared to women (80%, 69%, and 48.0% respectively, p\\textgreater0.05); a higher proportion of women had a CD4 count ≤200 compared to men and transgender women (17%, 8% and 5% respectively; p\\textgreater0.05). CONCLUSIONS: In this study, HIV-infected persons with recent incarceration in Washington, DC reported important risk factors and co-morbidities, yet the majority had access to HIV care and ART prior to, during, and after incarceration. Self-reported ART adherence was sub-optimal, and while there were not statistically significant differences, CJ-involved women appeared to be at greatest risk of poor HIV outcomes. TRIAL REGISTRATION: Registered on ClinicalTrials.gov on 10/16/2012. Reference number: NCT01721226.\n

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\n \n 2016\n \n \n (14)\n \n \n

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\n \n\n \n \n Nance, R.; Delaney, J. C.; Golin, C.; Wechsberg, W.; Cunningham, C.; Altice, F.; Christopoulos, K.; Knight, K.; Quan, V.; Gordon, M.; Springer, S.; Young, J.; Crane, P. K; Mayer, K. H; Mugavero, M. J; Del Rio, C.; Kronmal, R.; and Crane, H.\n\n\n \n \n \n \n \n Co-calibration of two self-reported measures of adherence to antiretroviral therapy.\n \n \n \n \n\n\n \n\n\n\n AIDS care, 29(4): 464–468. December 2016.\n \n\n\n\n
\n\n\n\n \n \n $\"Co-calibration$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n\n\n\n

@article{nance_co-calibration_2016,\n\ttitle = {Co-calibration of two self-reported measures of adherence to antiretroviral therapy},\n\tvolume = {29},\n\tissn = {0954-0121},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5291764/},\n\tdoi = {10.1080/09540121.2016.1263721},\n\tabstract = {Adherence to antiretroviral therapy (ART) is an important determinant of clinical success assessed in many HIV studies. Harmonizing adherence data from studies that use different measures is difficult without a co-calibration equation to convert between validated instruments. Our purpose was to co-calibrate two commonly used adherence measures: the AIDS Clinical Trials Group (ACTG) questionnaire and the Visual Analog Scale (VAS)., We used robust linear regression to develop a co-calibration equation in a clinical care cohort. The outcome was the 30-day VAS percentage of ART taken and the predictors were ACTG questions. We evaluated the equation’s goodness-of-fit in five STTR (Seek, Test, Treat, Retain) consortium studies where individuals completed both measures: 2 criminal justice; 2 international; and 1 other high-risk vulnerable population., We developed a three-phase decision rule to convert ACTG to VAS in 1045 participants. First, when the last missed dose on the ACTG was reported as {\\textgreater}30 days ago the VAS was set to 100\\% (N=582). Second, if “doses missed” was zero for all items, VAS was 100\\% (N=104). Third, among remaining participants (N=359), VAS was estimated as 96.8\\% minus 2.9\\% times the number of missed doses (“doses per day” was non-significant). Correlation between predicted and reported VAS was r=0.80 in the criminal justice group (N=446), r=0.46 in the international group (N=311), r=0.32 in the other vulnerable population (N=63), and r=0.66 overall. When outliers due to inversion of the VAS scale were excluded (n=25), these correlations were 0.88, 0.78, 0.80, and 0.86, respectively., We concluded that a simple decision rule and equation allowed us to co-calibrate between two widely used adherence measures thus combining data from studies with different instruments. This study highlighted issues with VAS inversions and its limitations as a single item. Combining studies using different instrument facilitates larger pooled data sets to address key research questions.},\n\tnumber = {4},\n\turldate = {2018-06-21},\n\tjournal = {AIDS care},\n\tauthor = {Nance, Robin and Delaney, J.A. Chris and Golin, Carol and Wechsberg, Wendee and Cunningham, Chinazo and Altice, Frederick and Christopoulos, Katerina and Knight, Kevin and Quan, Vu and Gordon, Michael and Springer, Sandra and Young, Jeremy and Crane, Paul K and Mayer, Kenneth H and Mugavero, Michael J and Del Rio, Carlos and Kronmal, Richard and Crane, Heidi},\n\tmonth = dec,\n\tyear = {2016},\n\tpmid = {27910703},\n\tpmcid = {PMC5291764},\n\tkeywords = {STTR Core},\n\tpages = {464--468},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

\n\n\n

\n Adherence to antiretroviral therapy (ART) is an important determinant of clinical success assessed in many HIV studies. Harmonizing adherence data from studies that use different measures is difficult without a co-calibration equation to convert between validated instruments. Our purpose was to co-calibrate two commonly used adherence measures: the AIDS Clinical Trials Group (ACTG) questionnaire and the Visual Analog Scale (VAS)., We used robust linear regression to develop a co-calibration equation in a clinical care cohort. The outcome was the 30-day VAS percentage of ART taken and the predictors were ACTG questions. We evaluated the equation’s goodness-of-fit in five STTR (Seek, Test, Treat, Retain) consortium studies where individuals completed both measures: 2 criminal justice; 2 international; and 1 other high-risk vulnerable population., We developed a three-phase decision rule to convert ACTG to VAS in 1045 participants. First, when the last missed dose on the ACTG was reported as \\textgreater30 days ago the VAS was set to 100% (N=582). Second, if “doses missed” was zero for all items, VAS was 100% (N=104). Third, among remaining participants (N=359), VAS was estimated as 96.8% minus 2.9% times the number of missed doses (“doses per day” was non-significant). Correlation between predicted and reported VAS was r=0.80 in the criminal justice group (N=446), r=0.46 in the international group (N=311), r=0.32 in the other vulnerable population (N=63), and r=0.66 overall. When outliers due to inversion of the VAS scale were excluded (n=25), these correlations were 0.88, 0.78, 0.80, and 0.86, respectively., We concluded that a simple decision rule and equation allowed us to co-calibrate between two widely used adherence measures thus combining data from studies with different instruments. This study highlighted issues with VAS inversions and its limitations as a single item. Combining studies using different instrument facilitates larger pooled data sets to address key research questions.\n

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\n \n\n \n \n Kiriazova, T.; Lunze, K.; Raj, A.; Bushara, N.; Blokhina, E.; Krupitsky, E.; Bridden, C.; Lioznov, D.; Samet, J. H.; and Gifford, A. L.\n\n\n \n \n \n \n \n “It is Easier for Me to Shoot Up”: Stigma, Abandonment, and Why HIV-positive Drug Users in Russia Fail to Link to HIV Care.\n \n \n \n \n\n\n \n\n\n\n AIDS care, 29(5): 559–563. November 2016.\n \n\n\n\n
\n\n\n\n \n \n $\"“It$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{kiriazova_it_2016,\n\ttitle = {“{It} is {Easier} for {Me} to {Shoot} {Up}”: {Stigma}, {Abandonment}, and {Why} {HIV}-positive {Drug} {Users} in {Russia} {Fail} to {Link} to {HIV} {Care}},\n\tvolume = {29},\n\tissn = {0954-0121},\n\tshorttitle = {“{It} is {Easier} for {Me} to {Shoot} {Up}”},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5350043/},\n\tdoi = {10.1080/09540121.2016.1259451},\n\tabstract = {Many HIV-positive people who inject drugs (PWID) globally are not receiving HIV care. This represents a major challenge among key populations to end the global HIV epidemic. This qualitative study explored the process and associated barriers of linking HIV-positive PWID who are in addiction treatment to HIV care in St. Petersburg, Russia. We conducted three focus groups and seven semi-structured interviews with participants in the LINC (“Linking Infectious and Narcology Care”) project at addiction and HIV hospitals in St. Petersburg. The sample consisted of 25 HIV-infected patients with opioid dependence and seven health care providers, including addiction and infectious disease physicians and case managers., A variety of intertwining factors influence effective engagement of PWID with HIV treatment. Stigma, problematic patient-provider relationships, and fragmented health care were the main challenges for HIV care initiation by PWID, which were further exacerbated by injection drug use. Effective linkage of PWID to HIV care requires acknowledging and addressing stigma’s role and different perspectives of patients and providers.},\n\tnumber = {5},\n\turldate = {2018-06-21},\n\tjournal = {AIDS care},\n\tauthor = {Kiriazova, Tetiana and Lunze, Karsten and Raj, Anita and Bushara, Natalia and Blokhina, Elena and Krupitsky, Evgeny and Bridden, Carly and Lioznov, Dmitry and Samet, Jeffrey H. and Gifford, Allen L.},\n\tmonth = nov,\n\tyear = {2016},\n\tpmid = {27871198},\n\tpmcid = {PMC5350043},\n\tpages = {559--563},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Glenn, M. C.; Sohler, N. L.; Starrels, J. L.; Maradiaga, J.; Jost, J. J.; Arnsten, J. H.; and Cunningham, C. O.\n\n\n \n \n \n \n \n Characteristics of methadone maintenance treatment patients prescribed opioid analgesics.\n \n \n \n \n\n\n \n\n\n\n Substance abuse, 37(3): 387–391. July 2016.\n \n\n\n\n
\n\n\n\n \n \n $\"Characteristics$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{glenn_characteristics_2016,\n\ttitle = {Characteristics of methadone maintenance treatment patients prescribed opioid analgesics},\n\tvolume = {37},\n\tissn = {0889-7077},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4935628/},\n\tdoi = {10.1080/08897077.2015.1135225},\n\tabstract = {Background\nOpioid analgesic use and disorders have dramatically increased among the general American population and those receiving methadone maintenance treatment (MMT). Most research among MMT patients focuses on opioid analgesics misuse or disorders; few studies focus on MMT patients prescribed opioid analgesics. We describe demographic, clinical, and substance use characteristics of MMT patients prescribed opioid analgesics and compare them to MMT patients not prescribed opioid analgesics.\n\nMethods\nWe conducted a cross-sectional secondary data analysis using screening interviews from a parent study. From 2012–2015, we recruited adults from 3 MMT Bronx clinics. Questionnaire data included: patterns of opioid analgesic use, substance use, comorbid illnesses, and demographic characteristics. Our main dependent variable was patients’ report of currently taking prescribed opioid analgesics. To compare characteristics between MMT patients prescribed and not prescribed opioid analgesics, we conducted chi-squared tests, t-tests, and Mann-Whitney U tests.\n\nResults\nOf 611 MMT patients, most reported chronic pain (62.0\\%), HCV infection (52.1\\%), and currently using illicit substances (64.2\\%). Of the 29.8\\% who reported currently taking prescribed opioid analgesics, most misused their opioid analgesics (57.5\\%). Patients prescribed (versus not prescribed) opioid analgesics were more likely to report HIV infection (aOR=1.6, 95\\% CI: 1.1–2.3) and chronic pain (aOR=7.6, 95\\% CI: 4.6–12.6).\n\nConclusion\nAmong MMT patients primarily in three Bronx clinics, nearly one-third reported taking prescribed opioid analgesics. Compared to patients not prescribed opioid analgesics, those prescribed opioid analgesics were more likely to report chronic pain and HIV infection. However, between these patients, there was no difference in illicit substance use. These findings highlight the complexity of addressing chronic pain in MMT patients.},\n\tnumber = {3},\n\turldate = {2018-04-25},\n\tjournal = {Substance abuse},\n\tauthor = {Glenn, Matthew C. and Sohler, Nancy L. and Starrels, Joanna L. and Maradiaga, Jeronimo and Jost, John J. and Arnsten, Julia H. and Cunningham, Chinazo O.},\n\tmonth = jul,\n\tyear = {2016},\n\tpmid = {26731299},\n\tpmcid = {PMC4935628},\n\tpages = {387--391},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Solomon, S. S.; Lucas, G. M.; Celentano, D. D.; McFall, A. M.; Ogburn, E.; Moulton, L. H.; Srikrishnan, A. K.; Kumar, M. S.; Anand, S.; Solomon, S.; and Mehta, S. H.\n\n\n \n \n \n \n \n Design of the Indian NCA study (Indian national collaboration on AIDS): a cluster randomized trial to evaluate the effectiveness of integrated care centers to improve HIV outcomes among men who have sex with men and persons who inject drugs in India.\n \n \n \n \n\n\n \n\n\n\n BMC Health Services Research, 16. November 2016.\n \n\n\n\n
\n\n\n\n \n \n $\"Design$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{solomon_design_2016,\n\ttitle = {Design of the {Indian} {NCA} study ({Indian} national collaboration on {AIDS}): a cluster randomized trial to evaluate the effectiveness of integrated care centers to improve {HIV} outcomes among men who have sex with men and persons who inject drugs in {India}},\n\tvolume = {16},\n\tissn = {1472-6963},\n\tshorttitle = {Design of the {Indian} {NCA} study ({Indian} national collaboration on {AIDS})},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5109686/},\n\tdoi = {10.1186/s12913-016-1905-5},\n\tabstract = {Background\nGlobally, men who have sex with men and people who inject drugs remain disproportionately affected by HIV, but they have not been the focus of prevention and treatment interventions in many resource-limited settings.\n\nMethods/Design\nThis cluster-randomized trial (conducted from June 2012 to June 2017), evaluates whether single-venue, integrated delivery of core HIV services to vulnerable high-risk populations improves service utilization and consequently, HIV testing and other outcomes along the HIV care continuum. Core services include: HIV counseling and testing, information, education and communication, condom distribution, needle and syringe exchange programs, opioid agonist therapy, management of sexually transmitted infections, tuberculosis screening, diagnosis, and treatment, and antiretroviral therapy. Stratified restricted randomization was used to allocate 22 Indian cities (10 men who have sex with men and 12 people who inject drugs sites) at a 1:1 ratio to either the intervention or control condition. Integrated care centers were scaled-up and implemented in the 11 intervention cities and outcomes will be assessed by pre- and post-intervention surveys at intervention and control sites. As men who have sex with men and people who inject drugs are hidden populations, with no sampling frame, respondent-driven sampling will be used to accrue samples for the two independent cross-sectional surveys.\n\nDiscussion\nFor an AIDS-free generation to be realized, prevention, care and treatment services need to reach all populations at risk for HIV infection. There is a clear gap in access to services among men who have sex with men and people who inject drugs. Trials need to be designed to optimize utilization of services in these populations.\n\nTrial registration\nClinicalTrials.gov Identifier: NCT01686750\n, Date of Registration: September 13, 2012\n\nElectronic supplementary material\nThe online version of this article (doi:10.1186/s12913-016-1905-5) contains supplementary material, which is available to authorized users.},\n\turldate = {2017-04-05},\n\tjournal = {BMC Health Services Research},\n\tauthor = {Solomon, Sunil S. and Lucas, Gregory M. and Celentano, David D. and McFall, Allison M. and Ogburn, Elizabeth and Moulton, Lawrence H. and Srikrishnan, Aylur K. and Kumar, M. Suresh and Anand, Santhanam and Solomon, Suniti and Mehta, Shruti H.},\n\tmonth = nov,\n\tyear = {2016},\n\tpmid = {27842543},\n\tpmcid = {PMC5109686},\n}\n\n\n\n\n\n\n\n\n\n\n\n

\n\n\n

\n Background Globally, men who have sex with men and people who inject drugs remain disproportionately affected by HIV, but they have not been the focus of prevention and treatment interventions in many resource-limited settings. Methods/Design This cluster-randomized trial (conducted from June 2012 to June 2017), evaluates whether single-venue, integrated delivery of core HIV services to vulnerable high-risk populations improves service utilization and consequently, HIV testing and other outcomes along the HIV care continuum. Core services include: HIV counseling and testing, information, education and communication, condom distribution, needle and syringe exchange programs, opioid agonist therapy, management of sexually transmitted infections, tuberculosis screening, diagnosis, and treatment, and antiretroviral therapy. Stratified restricted randomization was used to allocate 22 Indian cities (10 men who have sex with men and 12 people who inject drugs sites) at a 1:1 ratio to either the intervention or control condition. Integrated care centers were scaled-up and implemented in the 11 intervention cities and outcomes will be assessed by pre- and post-intervention surveys at intervention and control sites. As men who have sex with men and people who inject drugs are hidden populations, with no sampling frame, respondent-driven sampling will be used to accrue samples for the two independent cross-sectional surveys. Discussion For an AIDS-free generation to be realized, prevention, care and treatment services need to reach all populations at risk for HIV infection. There is a clear gap in access to services among men who have sex with men and people who inject drugs. Trials need to be designed to optimize utilization of services in these populations. Trial registration ClinicalTrials.gov Identifier: NCT01686750 , Date of Registration: September 13, 2012 Electronic supplementary material The online version of this article (doi:10.1186/s12913-016-1905-5) contains supplementary material, which is available to authorized users.\n

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\n \n\n \n \n Tsui, J. I.; Ko, S. C.; Krupitsky, E.; Lioznov, D.; Chaisson, C. E.; Gnatienko, N.; and Samet, J. H.\n\n\n \n \n \n \n \n Insights on the Russian HCV care cascade: minimal HCV treatment for HIV/HCV co-infected PWID in St. Petersburg.\n \n \n \n \n\n\n \n\n\n\n Hepatology, Medicine and Policy, 1: 13. October 2016.\n \n\n\n\n
\n\n\n\n \n \n $\"Insights$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{tsui_insights_2016,\n\ttitle = {Insights on the {Russian} {HCV} care cascade: minimal {HCV} treatment for {HIV}/{HCV} co-infected {PWID} in {St}. {Petersburg}},\n\tvolume = {1},\n\tissn = {2059-5166},\n\tshorttitle = {Insights on the {Russian} {HCV} care cascade},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5313079/},\n\tdoi = {10.1186/s41124-016-0020-x},\n\tabstract = {The human immunodeficiency virus (HIV) epidemic in Russia, driven by injection drug use, has seen a steady rise in the past two decades. Hepatitis C virus (HCV) infection is highly prevalent in people who inject drugs (PWID). The study aimed to describe the current frequency of HCV testing and treatment among HIV-infected PWID in St. Petersburg, Russia.},\n\turldate = {2016-10-31},\n\tjournal = {Hepatology, Medicine and Policy},\n\tauthor = {Tsui, Judith I. and Ko, Stephen C. and Krupitsky, Evgeny and Lioznov, Dmitry and Chaisson, Christine E. and Gnatienko, Natalia and Samet, Jeffrey H.},\n\tmonth = oct,\n\tyear = {2016},\n\tkeywords = {HCV, HIV, PWID, Russia},\n\tpages = {13},\n}\n\n\n\n

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\n \n\n \n \n Solomon, S. S.; Mehta, S. H; McFall, A. M; Srikrishnan, A. K; Saravanan, S.; Laeyendecker, O.; Balakrishnan, P.; Celentano, D. D; Solomon, S.; and Lucas, G. M\n\n\n \n \n \n \n \n Community viral load, antiretroviral therapy coverage, and HIV incidence in India: a cross-sectional, comparative study.\n \n \n \n \n\n\n \n\n\n\n The Lancet HIV. April 2016.\n \n\n\n\n
\n\n\n\n \n \n $\"Community$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{solomon_community_2016,\n\ttitle = {Community viral load, antiretroviral therapy coverage, and {HIV} incidence in {India}: a cross-sectional, comparative study},\n\tissn = {23523018},\n\tshorttitle = {Community viral load, antiretroviral therapy coverage, and {HIV} incidence in {India}},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4863069/},\n\tdoi = {10.1016/S2352-3018(16)00019-9},\n\tlanguage = {en},\n\turldate = {2016-03-15},\n\tjournal = {The Lancet HIV},\n\tauthor = {Solomon, Sunil Suhas and Mehta, Shruti H and McFall, Allison M and Srikrishnan, Aylur K and Saravanan, Shanmugam and Laeyendecker, Oliver and Balakrishnan, Pachamuthu and Celentano, David D and Solomon, Suniti and Lucas, Gregory M},\n\tmonth = apr,\n\tyear = {2016},\n}\n\n\n\n

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\n \n\n \n \n Gutman, R.; Sammartino, C. J.; Green, T. C.; and Montague, B. T.\n\n\n \n \n \n \n \n Error adjustments for file linking methods using encrypted unique client identifier (eUCI) with application to recently released prisoners who are HIV.\n \n \n \n \n\n\n \n\n\n\n Statistics in Medicine. January 2016.\n \n\n\n\n
\n\n\n\n \n \n $\"Error$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{gutman_error_2016,\n\ttitle = {Error adjustments for file linking methods using encrypted unique client identifier ({eUCI}) with application to recently released prisoners who are {HIV}},\n\tissn = {1097-0258},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4715569/},\n\tdoi = {10.1002/sim.6586},\n\tabstract = {Incarceration provides an opportunity to test for HIV, provide treatment such as highly active anti-retroviral therapy, as well as link infected persons to comprehensive HIV care upon their release. A key factor in assessing the success of a program that links released individuals to care is the time from release to receiving care in the community (linkage time). To estimate the linkage time, records from correction systems are linked to Ryan White Clinic data using encrypted Unique Client Identifier (eUCI). Most of the records that were linked using eUCI belong to the same individual; however, in some cases, it may link records incorrectly, or not identify records that should have been linked. We propose a Bayesian procedure that relies on the relationships between variables that appear in either of the data sources, as well as variables that exists in both to identify correctly linked records among all linked records. The procedure generates K datasets in which each pair of linked records is identified as a true link or a false link. The K datasets are analyzed independently, and the results are combined using Rubin's multiple imputation rules. A small validation dataset is used to examine different statistical models and to inform the prior distributions of the parameters. In comparison with previously proposed methods, the proposed method utilizes all of the available data and is both flexible and computationally efficient. In addition, this approach can be applied in other file linking applications. Copyright © 2015 John Wiley \\& Sons, Ltd.},\n\tlanguage = {ENG},\n\tjournal = {Statistics in Medicine},\n\tauthor = {Gutman, R. and Sammartino, C. J. and Green, T. C. and Montague, B. T.},\n\tmonth = jan,\n\tyear = {2016},\n\tpmid = {26202853},\n\tkeywords = {eUCI, file linking, mixture models, multiple imputation},\n}\n\n\n\n\n\n\n\n

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\n \n\n \n \n Gnatienko, N.; Han, S. C.; Krupitsky, E.; Blokhina, E.; Bridden, C.; Chaisson, C. E.; Cheng, D. M.; Walley, A. Y.; Raj, A.; and Samet, J. H.\n\n\n \n \n \n \n \n Linking Infectious and Narcology Care (LINC) in Russia: design, intervention and implementation protocol.\n \n \n \n \n\n\n \n\n\n\n Addiction Science & Clinical Practice, 11. May 2016.\n \n\n\n\n
\n\n\n\n \n \n $\"Linking$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{gnatienko_linking_2016,\n\ttitle = {Linking {Infectious} and {Narcology} {Care} ({LINC}) in {Russia}: design, intervention and implementation protocol},\n\tvolume = {11},\n\tissn = {1940-0632},\n\tshorttitle = {Linking {Infectious} and {Narcology} {Care} ({LINC}) in {Russia}},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4855723/},\n\tdoi = {10.1186/s13722-016-0058-5},\n\tabstract = {Background\nRussia and Eastern Europe have one of the fastest growing HIV epidemics in the world. While countries in this region have implemented HIV testing within addiction treatment systems, linkage to HIV care from these settings is not yet standard practice. The Linking Infectious and Narcology Care (LINC) intervention utilized peer-led strengths-based case management to motivate HIV-infected patients in addiction treatment to obtain HIV care. This paper describes the protocol of a randomized controlled trial evaluating the effectiveness of the LINC intervention in St. Petersburg, Russia.\n\nMethods/design\nParticipants (n = 349) were recruited from the inpatient wards at the City Addiction Hospital in St. Petersburg, Russia. After completing a baseline assessment, participants were randomly assigned to receive either the LINC intervention or standard of care. Participants returned for research assessments 6 and 12 months post-baseline. Primary outcomes were assessed via chart review at HIV treatment locations.\n\nDiscussion\nLINC holds the potential to offer an effective approach to coordinating HIV care for people who inject drugs in Russia. The LINC intervention utilizes existing systems of care in Russia, minimizing adoption of substantial infrastructure for implementation., Trial Registration NCT01612455},\n\turldate = {2017-03-13},\n\tjournal = {Addiction Science \\& Clinical Practice},\n\tauthor = {Gnatienko, Natalia and Han, Steve C. and Krupitsky, Evgeny and Blokhina, Elena and Bridden, Carly and Chaisson, Christine E. and Cheng, Debbie M. and Walley, Alexander Y. and Raj, Anita and Samet, Jeffrey H.},\n\tmonth = may,\n\tyear = {2016},\n\tpmid = {27141834},\n\tpmcid = {PMC4855723},\n}\n\n\n\n

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\n \n\n \n \n Herbeck, J.; and Tanser, F.\n\n\n \n \n \n \n \n Community viral load as an index of HIV transmission potential.\n \n \n \n \n\n\n \n\n\n\n The Lancet HIV, 3(4): e152–e154. April 2016.\n \n\n\n\n
\n\n\n\n \n \n $\"Community$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{herbeck_community_2016,\n\ttitle = {Community viral load as an index of {HIV} transmission potential},\n\tvolume = {3},\n\tissn = {2352-3018},\n\turl = {http://www.sciencedirect.com/science/article/pii/S2352301816000369},\n\tdoi = {10.1016/S2352-3018(16)00036-9},\n\tnumber = {4},\n\turldate = {2017-03-13},\n\tjournal = {The Lancet HIV},\n\tauthor = {Herbeck, Joshua and Tanser, Frank},\n\tmonth = apr,\n\tyear = {2016},\n\tpages = {e152--e154},\n}\n\n\n\n

\n\n\n\n

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\n \n\n \n \n McFall, A. M.; Mehta, S. H.; Srikrishnan, A. K.; Lucas, G. M.; Vasudevan, C. K.; Celentano, D. D.; Kumar, M. S.; Solomon, S.; and Solomon, S. S.\n\n\n \n \n \n \n \n Getting to 90: linkage to HIV care among men who have sex with men and people who inject drugs in India.\n \n \n \n \n\n\n \n\n\n\n AIDS care, 28(10): 1230–1239. October 2016.\n \n\n\n\n
\n\n\n\n \n \n $\"Getting$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{mcfall_getting_2016,\n\ttitle = {Getting to 90: linkage to {HIV} care among men who have sex with men and people who inject drugs in {India}},\n\tvolume = {28},\n\tissn = {0954-0121},\n\tshorttitle = {Getting to 90},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4972663/},\n\tdoi = {10.1080/09540121.2016.1168915},\n\tabstract = {UNAIDS set an ambitious target of “90-90-90” by 2020. The first 90 being 90\\% of those HIV-infected will be diagnosed; the second 90 being 90\\% of those diagnosed will be linked to medical care and on antiretroviral therapy (ART). While there has been dramatic improvement in HIV testing and ART use, substantial losses continue to occur at linkage-to-care following HIV diagnosis. Data on linkage among men who have sex with men (MSM) and people who inject drugs (PWID) are sparse, despite a greater burden of HIV in these populations. This cross-sectional study was conducted in 27 sites across India. Participants were recruited using respondent-driven sampling and had to be ≥18 years and self-identify as male and report sex with a man in the prior year (MSM) or injection drug use in the prior 2 years (PWID). Analyses were restricted to HIV-infected persons aware of their status. Linkage was defined as ever visiting a doctor for management of HIV after diagnosis. We explored factors that discriminated between those linked and not linked to care using multi-level logistic regression and area under the receiver operating curves (AUC), focusing on modifiable factors. Of 1726 HIV-infected persons aware of their status, 80\\% were linked to care. Modifiable factors around the time of diagnosis that best discriminated linkage included receiving assistance with HIV medical care (odds ratio [OR]: 10.0, 95\\% confidence interval [CI]): 5.6–18.2), disclosure of HIV-positive status (OR: 2.8; 95\\% CI: 2.4–6.1) and receiving information and counseling on management of HIV (OR: 2.3; 95\\% CI: 1.1–4.6). The AUC for these three factors together was 0.85, higher than other combinations of factors. We identified three simple modifiable factors around the time of diagnosis that could facilitate linkage to care among MSM and PWID in low- and middle-income countries to achieve UNAIDS targets.},\n\tnumber = {10},\n\turldate = {2017-03-13},\n\tjournal = {AIDS care},\n\tauthor = {McFall, Allison M. and Mehta, Shruti H. and Srikrishnan, Aylur K. and Lucas, Gregory M. and Vasudevan, Canjeevaram K. and Celentano, David D. and Kumar, Muniratnam S. and Solomon, Suniti and Solomon, Sunil S.},\n\tmonth = oct,\n\tyear = {2016},\n\tpmid = {27054274},\n\tpmcid = {PMC4972663},\n\tpages = {1230--1239},\n}\n\n\n\n

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\n \n\n \n \n Golin, C. E.; Knight, K.; Carda-Auten, J.; Gould, M.; Groves, J.; L.White, B.; Bradley-Bull, S.; Amola, K.; Fray, N.; Rosen, D. L.; Mugavaro, M. J.; Pence, B. W.; Flynn, P. M.; and Wohl, D.\n\n\n \n \n \n \n \n Individuals motivated to participate in adherence, care and treatment (imPACT): development of a multi-component intervention to help HIV-infected recently incarcerated individuals link and adhere to HIV care.\n \n \n \n \n\n\n \n\n\n\n BMC Public Health, 16(1). September 2016.\n \n\n\n\n
\n\n\n\n \n \n $\"Individuals$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{golin_individuals_2016,\n\ttitle = {Individuals motivated to participate in adherence, care and treatment ({imPACT}): development of a multi-component intervention to help {HIV}-infected recently incarcerated individuals link and adhere to {HIV} care},\n\tvolume = {16},\n\tissn = {1471-2458},\n\tshorttitle = {Individuals motivated to participate in adherence, care and treatment ({imPACT})},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5011897/},\n\tdoi = {10.1186/s12889-016-3511-1},\n\tabstract = {Background\nPolicy-makers promote a seek, test, treat and retain (STTR) strategy to expand HIV testing, support linkage and engagement in care, and enhance the continuous use of antiretroviral therapy for those HIV-infected. This HIV prevention strategy is particularly appropriate in correctional settings where HIV screening and treatment are routinely available yet many HIV-infected individuals have difficulty sustaining sufficient linkage and engagement in care, disease management, and viral suppression after prison release.\n\nMethods/design\nOur research team developed Project imPACT (individuals motivated to Participate in Adherence, Care and Treatment), a multi-component approach for HIV-Infected recently incarcerated individuals that specifically targets their care linkage, retention, and medication adherence by addressing multiple barriers to care engagement after release. The ultimate goals of this intervention are to improve the health of HIV-infected individuals recently released from prison and reduce HIV transmission to their communities by maintaining viral suppression. This paper describes the intervention and technology development processes, based on best practices for intervention development and process evaluation. These processes included: 1) identifying the target population; 2) clarifying the theoretical basis for intervention design; 3) describing features of its foundational interventions; 4) conducting formative qualitative research; 5) integrating and adapting foundational interventions to create and refine intervention content based on target audience feedback. These stages along with the final intervention product are described in detail. The intervention is currently being evaluation and a two arm randomized, controlled trial in two US state prison systems.\n\nDiscussion\nBased on a literature review, qualitative research, integration of proven interventions and behavioral theory, the final imPACT intervention focused on the transition period two to three months before and three months after prison release. It emphasized pre-release readiness, pre- and post-release supportive non-judgmental counseling, linking individuals to a HIV care clinic and technological supports through videos and text messages. This article provides a useful model for how researchers can develop, test, and refine multi-component interventions to address HIV care linkage, retention and adherence.\n\nClinical trial registration\nNCT01629316, first registered 6-4-2012; last updated 6-9-2015.},\n\tnumber = {1},\n\turldate = {2017-03-13},\n\tjournal = {BMC Public Health},\n\tauthor = {Golin, Carol E. and Knight, Kevin and Carda-Auten, Jessica and Gould, Michele and Groves, Jennifer and L.White, Becky and Bradley-Bull, Steve and Amola, Kemi and Fray, Niasha and Rosen, David L. and Mugavaro, Michael J. and Pence, Brian W. and Flynn, Patrick M. and Wohl, David},\n\tmonth = sep,\n\tyear = {2016},\n\tpmid = {27596559},\n\tpmcid = {PMC5011897},\n}\n\n\n\n

\n\n\n

\n Background Policy-makers promote a seek, test, treat and retain (STTR) strategy to expand HIV testing, support linkage and engagement in care, and enhance the continuous use of antiretroviral therapy for those HIV-infected. This HIV prevention strategy is particularly appropriate in correctional settings where HIV screening and treatment are routinely available yet many HIV-infected individuals have difficulty sustaining sufficient linkage and engagement in care, disease management, and viral suppression after prison release. Methods/design Our research team developed Project imPACT (individuals motivated to Participate in Adherence, Care and Treatment), a multi-component approach for HIV-Infected recently incarcerated individuals that specifically targets their care linkage, retention, and medication adherence by addressing multiple barriers to care engagement after release. The ultimate goals of this intervention are to improve the health of HIV-infected individuals recently released from prison and reduce HIV transmission to their communities by maintaining viral suppression. This paper describes the intervention and technology development processes, based on best practices for intervention development and process evaluation. These processes included: 1) identifying the target population; 2) clarifying the theoretical basis for intervention design; 3) describing features of its foundational interventions; 4) conducting formative qualitative research; 5) integrating and adapting foundational interventions to create and refine intervention content based on target audience feedback. These stages along with the final intervention product are described in detail. The intervention is currently being evaluation and a two arm randomized, controlled trial in two US state prison systems. Discussion Based on a literature review, qualitative research, integration of proven interventions and behavioral theory, the final imPACT intervention focused on the transition period two to three months before and three months after prison release. It emphasized pre-release readiness, pre- and post-release supportive non-judgmental counseling, linking individuals to a HIV care clinic and technological supports through videos and text messages. This article provides a useful model for how researchers can develop, test, and refine multi-component interventions to address HIV care linkage, retention and adherence. Clinical trial registration NCT01629316, first registered 6-4-2012; last updated 6-9-2015.\n

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\n \n\n \n \n Beckwith, C. G.; Kurth, A. E.; Bazerman, L. B.; Patry, E. J.; Cates, A.; Tran, L.; Noska, A.; and Kuo, I.\n\n\n \n \n \n \n \n A pilot study of rapid hepatitis C virus testing in the Rhode Island Department of Corrections.\n \n \n \n \n\n\n \n\n\n\n Journal of Public Health (Oxford, England), 38(1): 130–137. March 2016.\n \n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{beckwith_pilot_2016,\n\ttitle = {A pilot study of rapid hepatitis {C} virus testing in the {Rhode} {Island} {Department} of {Corrections}},\n\tvolume = {38},\n\tissn = {1741-3842},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4750523/},\n\tdoi = {10.1093/pubmed/fdv023},\n\tabstract = {Background\nThe correctional population bears a heavy burden of hepatitis C virus (HCV) infection necessitating expansion of HCV testing and treatment opportunities. Rapid HCV testing provides point-of-care antibody results and may be ideal for correctional facilities, particularly jails, where persons are often incarcerated for short periods of time, yet feasibility has not been established.\n\nMethods\nWe conducted a pilot study of a rapid HCV testing algorithm among short-term inmates with unknown HCV status. Participants completed a questionnaire, viewed an informational video and underwent rapid HCV testing and confirmatory testing, when indicated. Persons with chronic infection were referred to community care after release. Baseline characteristics, risk behaviors, test results and linkage were examined by descriptive analyses.\n\nResults\nTwo hundred and fifty-two inmates were enrolled and 249 completed all study activities. Twenty-five participants (10\\%) had reactive rapid tests and 23 (92\\%) completed confirmatory testing. 15/23 (65\\%) had detectable HCV RNA, but only 4 linked to care after release. Persons with reactive HCV tests were more likely to be White (P = 0.01) and to have ever injected (P {\\textless} 0.0001) and/or recently injected (P {\\textless} 0.0001) drugs.\n\nConclusions\nRapid HCV testing within jails is feasible, identifies previously unrecognized cases of HCV infection, and implementation should be considered. Low rates of linkage to care after release remain a barrier to care.},\n\tnumber = {1},\n\turldate = {2017-03-13},\n\tjournal = {Journal of Public Health (Oxford, England)},\n\tauthor = {Beckwith, Curt G. and Kurth, Ann E. and Bazerman, Lauri B. and Patry, Emily J. and Cates, Alice and Tran, Liem and Noska, Amanda and Kuo, Irene},\n\tmonth = mar,\n\tyear = {2016},\n\tpmid = {25736438},\n\tpmcid = {PMC4750523},\n\tpages = {130--137},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Gwadz, M.; Cleland, C. M.; Kutnick, A.; Leonard, N. R.; Ritchie, A. S.; Lynch, L.; Banfield, A.; McCright-Gill, T.; del Olmo, M.; and Martinez, B.\n\n\n \n \n \n \n \n Factors Associated with Recent HIV Testing among Heterosexuals at High Risk for HIV Infection in New York City.\n \n \n \n \n\n\n \n\n\n\n Frontiers in Public Health, 4. April 2016.\n \n\n\n\n
\n\n\n\n \n \n $\"Factors$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{gwadz_factors_2016,\n\ttitle = {Factors {Associated} with {Recent} {HIV} {Testing} among {Heterosexuals} at {High} {Risk} for {HIV} {Infection} in {New} {York} {City}},\n\tvolume = {4},\n\tissn = {2296-2565},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4846660/},\n\tdoi = {10.3389/fpubh.2016.00076},\n\tabstract = {Background\nThe Centers for Disease Control and Prevention recommends persons at high risk for HIV infection in the United States receive annual HIV testing to foster early HIV diagnosis and timely linkage to health care. Heterosexuals make up a significant proportion of incident HIV infections ({\\textgreater}25\\%) but test for HIV less frequently than those in other risk categories. Yet factors that promote or impede annual HIV testing among heterosexuals are poorly understood. The present study examines individual/attitudinal-, social-, and structural-level factors associated with past-year HIV testing among heterosexuals at high risk for HIV.\n\nMethods\nParticipants were African-American/Black and Hispanic heterosexual adults (N = 2307) residing in an urban area with both high poverty and HIV prevalence rates. Participants were recruited by respondent-driven sampling in 2012–2015 and completed a computerized structured assessment battery covering background factors, multi-level putative facilitators of HIV testing, and HIV testing history. Separate logistic regression analysis for males and females identified factors associated with past-year HIV testing.\n\nResults\nParticipants were mostly male (58\\%), African-American/Black (75\\%), and 39 years old on average (SD = 12.06 years). Lifetime homelessness (54\\%) and incarceration (62\\%) were common. Half reported past-year HIV testing (50\\%) and 37\\% engaged in regular, annual HIV testing. Facilitators of HIV testing common to both genders included sexually transmitted infection (STI) testing or STI diagnosis, peer norms supporting HIV testing, and HIV testing access. Among women, access to general medical care and extreme poverty further predicted HIV testing, while recent drug use reduced the odds of past-year HIV testing. Among men, past-year HIV testing was also associated with lifetime incarceration and substance use treatment.\n\nConclusion\nThe present study identified gaps in rates of HIV testing among heterosexuals at high risk for HIV, and both common and gender-specific facilitators of HIV testing. Findings suggest a number of avenues for increasing HIV testing rates, including increasing the number and types of settings offering high-quality HIV testing; promoting STI as well as HIV testing; better integrating STI and HIV testing systems; implementing peer-driven social/behavioral intervention approaches to harness the positive influence of social networks and reduce unfavorable shared peer norms; and specialized approaches for women who use drugs.},\n\turldate = {2017-03-13},\n\tjournal = {Frontiers in Public Health},\n\tauthor = {Gwadz, Marya and Cleland, Charles M. and Kutnick, Alexandra and Leonard, Noelle R. and Ritchie, Amanda S. and Lynch, Laura and Banfield, Angela and McCright-Gill, Talaya and del Olmo, Montserrat and Martinez, Belkis},\n\tmonth = apr,\n\tyear = {2016},\n\tpmid = {27200330},\n\tpmcid = {PMC4846660},\n}\n\n\n\n\n\n\n\n\n\n\n\n

\n\n\n

\n Background The Centers for Disease Control and Prevention recommends persons at high risk for HIV infection in the United States receive annual HIV testing to foster early HIV diagnosis and timely linkage to health care. Heterosexuals make up a significant proportion of incident HIV infections (\\textgreater25%) but test for HIV less frequently than those in other risk categories. Yet factors that promote or impede annual HIV testing among heterosexuals are poorly understood. The present study examines individual/attitudinal-, social-, and structural-level factors associated with past-year HIV testing among heterosexuals at high risk for HIV. Methods Participants were African-American/Black and Hispanic heterosexual adults (N = 2307) residing in an urban area with both high poverty and HIV prevalence rates. Participants were recruited by respondent-driven sampling in 2012–2015 and completed a computerized structured assessment battery covering background factors, multi-level putative facilitators of HIV testing, and HIV testing history. Separate logistic regression analysis for males and females identified factors associated with past-year HIV testing. Results Participants were mostly male (58%), African-American/Black (75%), and 39 years old on average (SD = 12.06 years). Lifetime homelessness (54%) and incarceration (62%) were common. Half reported past-year HIV testing (50%) and 37% engaged in regular, annual HIV testing. Facilitators of HIV testing common to both genders included sexually transmitted infection (STI) testing or STI diagnosis, peer norms supporting HIV testing, and HIV testing access. Among women, access to general medical care and extreme poverty further predicted HIV testing, while recent drug use reduced the odds of past-year HIV testing. Among men, past-year HIV testing was also associated with lifetime incarceration and substance use treatment. Conclusion The present study identified gaps in rates of HIV testing among heterosexuals at high risk for HIV, and both common and gender-specific facilitators of HIV testing. Findings suggest a number of avenues for increasing HIV testing rates, including increasing the number and types of settings offering high-quality HIV testing; promoting STI as well as HIV testing; better integrating STI and HIV testing systems; implementing peer-driven social/behavioral intervention approaches to harness the positive influence of social networks and reduce unfavorable shared peer norms; and specialized approaches for women who use drugs.\n

\n\n\n

\n \n\n \n \n Gwadz, M.; Cleland, C. M.; Jenness, S. M.; Silverman, E.; Hagan, H.; Ritchie, A. S.; Leonard, N. R.; McCright-Gill, T.; Martinez, B.; Swain, Q.; Kutnick, A.; and Sherpa, D.\n\n\n \n \n \n \n \n Exploring Factors Associated with Recent HIV Testing among Heterosexuals at High Risk for HIV Infection Recruited with Venue-based Sampling.\n \n \n \n \n\n\n \n\n\n\n Journal of AIDS & clinical research, 7(2). February 2016.\n \n\n\n\n
\n\n\n\n \n \n $\"Exploring$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{gwadz_exploring_2016,\n\ttitle = {Exploring {Factors} {Associated} with {Recent} {HIV} {Testing} among {Heterosexuals} at {High} {Risk} for {HIV} {Infection} {Recruited} with {Venue}-based {Sampling}},\n\tvolume = {7},\n\tissn = {2155-6113},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4836844/},\n\tdoi = {10.4172/2155-6113.1000544},\n\tabstract = {Annual HIV testing is recommended for high-risk populations in the United States, to identify HIV infections early and provide timely linkage to treatment. However, heterosexuals at high risk for HIV, due to their residence in urban areas of high poverty and elevated HIV prevalence, test for HIV less frequently than other risk groups, and late diagnosis of HIV is common. Yet the factors impeding HIV testing in this group, which is predominantly African American/Black and Latino/Hispanic, are poorly understood. The present study addresses this gap. Using a systematic community-based sampling method, venue-based sampling (VBS), we estimate rates of lifetime and recent (past year) HIV testing among high-risk heterosexuals (HRH), and explore a set of putative multi-level barriers to and facilitators of recent testing, by gender. Participants were 338 HRH African American/Black and Latino/Hispanic adults recruited using VBS, who completed a computerized structured assessment battery guided by the Theory of Triadic Influence, comprised of reliable/valid measures on socio-demographic characteristics, HIV testing history, and multi-level barriers to HIV testing. Logistic regression analysis was used to identify factors associated with HIV testing within the past year. Most HRH had tested at least once (94\\%), and more than half had tested within the past year (58\\%), but only 37\\% tested annually. In both men and women, the odds of recent testing were similar and associated with structural factors (better access to testing) and sexually transmitted infection (STI) testing and diagnosis. Thus VBS identified serious gaps in rates of annual HIV testing among HRH. Improvements in access to high-quality HIV testing and leveraging of STI testing are needed to increase the proportion of HRH testing annually for HIV. Such improvements could increase early detection of HIV, improve the long-term health of individuals, and reduce HIV transmission by increasing rates of viral suppression.},\n\tnumber = {2},\n\turldate = {2017-03-13},\n\tjournal = {Journal of AIDS \\& clinical research},\n\tauthor = {Gwadz, Marya and Cleland, Charles M. and Jenness, Samuel M. and Silverman, Elizabeth and Hagan, Holly and Ritchie, Amanda S. and Leonard, Noelle R. and McCright-Gill, Talaya and Martinez, Belkis and Swain, Quentin and Kutnick, Alexandra and Sherpa, Dawa},\n\tmonth = feb,\n\tyear = {2016},\n\tpmid = {27104046},\n\tpmcid = {PMC4836844},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n Annual HIV testing is recommended for high-risk populations in the United States, to identify HIV infections early and provide timely linkage to treatment. However, heterosexuals at high risk for HIV, due to their residence in urban areas of high poverty and elevated HIV prevalence, test for HIV less frequently than other risk groups, and late diagnosis of HIV is common. Yet the factors impeding HIV testing in this group, which is predominantly African American/Black and Latino/Hispanic, are poorly understood. The present study addresses this gap. Using a systematic community-based sampling method, venue-based sampling (VBS), we estimate rates of lifetime and recent (past year) HIV testing among high-risk heterosexuals (HRH), and explore a set of putative multi-level barriers to and facilitators of recent testing, by gender. Participants were 338 HRH African American/Black and Latino/Hispanic adults recruited using VBS, who completed a computerized structured assessment battery guided by the Theory of Triadic Influence, comprised of reliable/valid measures on socio-demographic characteristics, HIV testing history, and multi-level barriers to HIV testing. Logistic regression analysis was used to identify factors associated with HIV testing within the past year. Most HRH had tested at least once (94%), and more than half had tested within the past year (58%), but only 37% tested annually. In both men and women, the odds of recent testing were similar and associated with structural factors (better access to testing) and sexually transmitted infection (STI) testing and diagnosis. Thus VBS identified serious gaps in rates of annual HIV testing among HRH. Improvements in access to high-quality HIV testing and leveraging of STI testing are needed to increase the proportion of HRH testing annually for HIV. Such improvements could increase early detection of HIV, improve the long-term health of individuals, and reduce HIV transmission by increasing rates of viral suppression.\n

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\n \n 2015\n \n \n (15)\n \n \n

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\n \n\n \n \n Lorvick, J.; Comfort, M. L; Krebs, C. P; and Kral, A. H\n\n\n \n \n \n \n \n Health service use and social vulnerability in a community-based sample of women on probation and parole, 2011–2013.\n \n \n \n \n\n\n \n\n\n\n Health & Justice, 3. June 2015.\n \n\n\n\n
\n\n\n\n \n \n $\"Health$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{lorvick_health_2015,\n\ttitle = {Health service use and social vulnerability in a community-based sample of women on probation and parole, 2011–2013},\n\tvolume = {3},\n\tissn = {2194-7899},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5151512/},\n\tdoi = {10.1186/s40352-015-0024-4},\n\tabstract = {Background\nMost women involved in the criminal justice system are not incarcerated, but rather on probation or parole. We examined the receipt of health services and social vulnerability among women on parole or probation in the past year.\n\nMethods\nIn a community-based sample of 776 women who use crack cocaine or injection drugs, we compared those who had been on probation or parole in the past year with those who had no criminal justice involvement in the past year.\n\nResults\nWomen recently on probation or people were no more likely have health insurance, or to receive most health services, than women not in the criminal justice system. In addition, we found social vulnerabilities that contribute to poor health to be significantly more prevalent among women on probation or parole.\n\nConclusions\nThere is a missed opportunity to address health and social needs of women on probation or parole.},\n\turldate = {2018-11-20},\n\tjournal = {Health \\& Justice},\n\tauthor = {Lorvick, Jennifer and Comfort, Megan L and Krebs, Christopher P and Kral, Alex H},\n\tmonth = jun,\n\tyear = {2015},\n\tpmid = {null},\n\tpmcid = {PMC5151512},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Chandler, R. K.; Kahana, S. Y.; Fletcher, B.; Jones, D.; Finger, M. S.; Aklin, W. M.; Hamill, K.; and Webb, C.\n\n\n \n \n \n \n \n Data Collection and Harmonization in HIV Research: The Seek, Test, Treat, and Retain Initiative at the National Institute on Drug Abuse.\n \n \n \n \n\n\n \n\n\n\n American Journal of Public Health, 105(12): 2416–2422. December 2015.\n \n\n\n\n
\n\n\n\n \n \n $\"Data$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n\n\n\n

@article{chandler_data_2015,\n\ttitle = {Data {Collection} and {Harmonization} in {HIV} {Research}: {The} {Seek}, {Test}, {Treat}, and {Retain} {Initiative} at the {National} {Institute} on {Drug} {Abuse}},\n\tvolume = {105},\n\tissn = {0090-0036},\n\tshorttitle = {Data {Collection} and {Harmonization} in {HIV} {Research}},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4638253/},\n\tdoi = {10.2105/AJPH.2015.302788},\n\tabstract = {Large-scale, multisite data sets offer the potential for exploring the public health benefits of biomedical interventions. Data harmonization is an emerging strategy to increase the comparability of research data collected across independent studies, enabling research questions to be addressed beyond the capacity of any individual study., The National Institute on Drug Abuse recently implemented this novel strategy to prospectively collect and harmonize data across 22 independent research studies developing and empirically testing interventions to effectively deliver an HIV continuum of care to diverse drug-abusing populations., We describe this data collection and harmonization effort, collectively known as the Seek, Test, Treat, and Retain Data Collection and Harmonization Initiative, which can serve as a model applicable to other research endeavors.},\n\tnumber = {12},\n\turldate = {2018-06-21},\n\tjournal = {American Journal of Public Health},\n\tauthor = {Chandler, Redonna K. and Kahana, Shoshana Y. and Fletcher, Bennett and Jones, Dionne and Finger, Matthew S. and Aklin, Will M. and Hamill, Kathleen and Webb, Candace},\n\tmonth = dec,\n\tyear = {2015},\n\tpmid = {26469642},\n\tpmcid = {PMC4638253},\n\tkeywords = {STTR Core},\n\tpages = {2416--2422},\n}\n\n\n\n\n\n\n\n

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\n \n\n \n \n Springer, S. A.; Altice, F. L.; Brown, S.; and Di Paola, A.\n\n\n \n \n \n \n \n Correlates of Retention on Extended-Release Naltrexone among Persons Living with HIV Infection Transitioning to the Community from the Criminal Justice System.\n \n \n \n \n\n\n \n\n\n\n Drug and alcohol dependence, 157: 158–165. December 2015.\n \n\n\n\n
\n\n\n\n \n \n $\"Correlates$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{springer_correlates_2015,\n\ttitle = {Correlates of {Retention} on {Extended}-{Release} {Naltrexone} among {Persons} {Living} with {HIV} {Infection} {Transitioning} to the {Community} from the {Criminal} {Justice} {System}},\n\tvolume = {157},\n\tissn = {0376-8716},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4675147/},\n\tdoi = {10.1016/j.drugalcdep.2015.10.023},\n\tabstract = {Background\nThe acceptability of and retention on extended-release naltrexone\n(XR-NTX), an FDA-approved medication for the treatment of alcohol and opioid\nuse disorders, among persons living with HIV disease (PLH) under criminal\njustice setting (CJS) supervision has not been evaluated to date.\n\nMethods\nTwo double-blind placebo-controlled randomized trials of XR-NTX for\ninmates with HIV disease transitioning to the community with (1) alcohol use\ndisorders (AUDs) or (2) opioid use disorders, are underway. Reasons for not\naccepting XR-NTX and an evaluation of differences in demographic features\nbetween those who were retained on study drug and those who did not return\nfor their second injection post-release are discussed.\n\nResults\n70\\% of eligible persons consented to participate; almost\n90\\% received their first injection; and almost 60\\% returned\nfor their second injection after release. Variables found to be associated\n(p{\\textless}0.10) with returning for the second injection included: not\nmeeting criteria for hazardous drinking (p=0.035; OR 0.424 (CI\n0.191–0.941)); being prescribed antiretroviral therapy (p=0.068; OR\n2.170 (CI 0.943–4.992)); expressing experiencing serious depression\n30 days prior to incarceration (p=0.068; OR 1.889 (CI 0.955–3.737));\nnot having a positive cocaine urine screen on the day of release (DOR)\n(p=0.011; OR 0.258 (CI 0.091–0.729)); and not meeting criteria for\nan AUD plus any substance use disorder (p=0.068; OR 0.521\n(CI 0.259–1.048)). Only positive cocaine urine test on DOR was\nstatistically significant after multivariate regression analyses (p=0.005;\nOR 0.207 (CI 0.068–0.623)).\n\nConclusion\nCJS based XR-NTX programs are highly acceptable among PLH, however\nretention on XR-NTX after release is negatively impacted by relapse to\ncocaine use.},\n\turldate = {2017-03-13},\n\tjournal = {Drug and alcohol dependence},\n\tauthor = {Springer, Sandra A. and Altice, Frederick L. and Brown, Shan-Estelle and Di Paola, Angela},\n\tmonth = dec,\n\tyear = {2015},\n\tpmid = {26560326},\n\tpmcid = {PMC4675147},\n\tpages = {158--165},\n}\n\n\n\n

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\n \n\n \n \n Comfort, M.; Lopez, A. M.; Powers, C.; Kral, A. H.; and Lorvick, J.\n\n\n \n \n \n \n \n How Institutions Deprive: Ethnography, Social Work, and Interventionist Ethics Among the Hypermarginalized.\n \n \n \n \n\n\n \n\n\n\n RSF, 1(1): 100–119. November 2015.\n \n\n\n\n
\n\n\n\n \n \n $\"How$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{comfort_how_2015,\n\ttitle = {How {Institutions} {Deprive}: {Ethnography}, {Social} {Work}, and {Interventionist} {Ethics} {Among} the {Hypermarginalized}},\n\tvolume = {1},\n\tissn = {2377-8253},\n\tshorttitle = {How {Institutions} {Deprive}},\n\turl = {http://www.rsfjournal.org/doi/abs/10.7758/RSF.2015.1.1.06},\n\tdoi = {10.7758/RSF.2015.1.1.06},\n\tabstract = {Hypermarginalized populations, such as homeless drug users with acute health problems, are subject to multiple intersecting adversities that result in social exclusion and chronic suffering. Despite this population's high need for health and social services, institutions provide services that are fragmented and often punitive, contributing to further marginality. In this article, we present a hybrid methodological approach that combines clinical social work and ethnography in a study of intensive case management for HIV-positive indigent adults in Oakland, California. We investigate two primary research questions. First, we consider the challenges this population faces in navigating institutions to meet their basic needs, and we demonstrate how organizational irrationality has severe consequences for this population. Second, we grapple with the question of how to ethically engage hypermarginalized participants in research by presenting a clinically informed intervention that is responsive to individual vulnerabilities and also enhances our understanding of institutional failure.},\n\tnumber = {1},\n\turldate = {2016-03-15},\n\tjournal = {RSF},\n\tauthor = {Comfort, Megan and Lopez, Andrea M. and Powers, Christina and Kral, Alex H. and Lorvick, Jennifer},\n\tmonth = nov,\n\tyear = {2015},\n\tpages = {100--119},\n}\n\n\n\n

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\n \n\n \n \n Dennis, A. C.; Barrington, C.; Hino, S.; Gould, M.; Wohl, D.; and Golin, C. E.\n\n\n \n \n \n \n \n “You’re in a world of chaos”: Experiences accessing HIV care and adhering to medications after incarceration.\n \n \n \n \n\n\n \n\n\n\n The Journal of the Association of Nurses in AIDS Care : JANAC, 26(5): 542–555. September 2015.\n \n\n\n\n
\n\n\n\n \n \n $\"“You’re$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{dennis_youre_2015,\n\ttitle = {“{You}’re in a world of chaos”: {Experiences} accessing {HIV} care and adhering to medications after incarceration},\n\tvolume = {26},\n\tissn = {1055-3290},\n\tshorttitle = {“{You}’re in a world of chaos”},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4540691/},\n\tdoi = {10.1016/j.jana.2015.06.001},\n\tabstract = {Most HIV-infected inmates leave prison with a suppressed viral load; many, however, become disconnected from care and non-adherent to medications during reentry to community life. In this secondary data analysis of focus groups (N = 6) and in-depth interviews (N = 9) with 46 formerly incarcerated HIV-infected people during reentry, we used an inductive analytic approach to explore the interplay between individual, interpersonal, community, and structural factors and HIV management. Participants described barriers and facilitators to care engagement and adherence at each of these 4 levels, as well as a milieu of HIV and incarceration-related stigma and discrimination. The constellation of barriers and facilitators created competing demands and a sense of chaos in participants’ lives, which led them to address reentry-related basic needs (e.g., housing, food) before health care needs. Interventions that simultaneously address multiple levels, including augmenting employment and housing opportunities, enhancing social support, and reducing stigma, are needed.},\n\tnumber = {5},\n\turldate = {2017-03-13},\n\tjournal = {The Journal of the Association of Nurses in AIDS Care : JANAC},\n\tauthor = {Dennis, Alexis C. and Barrington, Clare and Hino, Sayaka and Gould, Michele and Wohl, David and Golin, Carol E.},\n\tmonth = sep,\n\tyear = {2015},\n\tpmid = {26188413},\n\tpmcid = {PMC4540691},\n\tpages = {542--555},\n}\n\n\n\n

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\n \n\n \n \n Solomon, S. S.; Mehta, S. H; Srikrishnan, A. K; Solomon, S.; McFall, A. M.; Laeyendecker, O.; Celentano, D. D; Iqbal, S. H; Anand, S.; Vasudevan, C. K; Saravanan, S.; Lucas, G. M; Kumar, M. S; Sulkowski, M. S; and Quinn, T. C\n\n\n \n \n \n \n \n High burden of HCV disease and poor access to HCV services among people who inject drugs in India: A cross-sectional study among 14,481 drug users across India.\n \n \n \n \n\n\n \n\n\n\n The Lancet. Infectious diseases, 15(1): 36–45. January 2015.\n \n\n\n\n
\n\n\n\n \n \n $\"High$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{solomon_high_2015,\n\ttitle = {High burden of {HCV} disease and poor access to {HCV} services among people who inject drugs in {India}: {A} cross-sectional study among 14,481 drug users across {India}},\n\tvolume = {15},\n\tissn = {1473-3099},\n\tshorttitle = {High burden of {HCV} disease and poor access to {HCV} services among people who inject drugs in {India}},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4503257/},\n\tdoi = {10.1016/S1473-3099(14)71045-X},\n\tabstract = {Background\nGlobally, 90\\% of HCV-infected individuals reside in resource-limited settings (RLS). We characterized the prevalence of HCV, HIV/HCV co-infection, and the HCV care continuum among people who inject drugs (PWID) in India.\n\nMethods\n14,481 PWID were sampled from 15 cities throughout India using respondent-driven sampling (RDS) from January–December 2013. HCV prevalence was estimated by the presence of anti-HCV antibodies incorporating RDS weights. HCV care continuum outcomes were self-reported except for viral clearance among treatment-experienced participants.\n\nFindings\nMedian age was 30 years and 13,608/14,449 (92·4\\%) were male. Overall weighted HCV prevalence was 37·2\\% (5,777/14,447); HIV/HCV co-infection prevalence was 13·2\\% (2,085/14,435). Correlates of HCV infection included higher lifetime injection frequency, HIV positivity, and a higher prevalence of persons with HIV RNA {\\textgreater} 1000 copies/ml in the community. Of 5,777 HCV antibody positive PWID, 440 (5·5\\%) were aware of their status, 225 (3·0\\%) had seen a doctor for their HCV, 79 (1·4\\%) had taken HCV treatment, and 18 (0·4\\%) had undetectable HCV RNA. Overall, 6,138/12,128 (50·5\\%) did not get tested for HCV because they had never heard of HCV. Among the 5,777 HCV antibody positives, 2,086 (34·4\\%) reported harmful/hazardous alcohol use of whom 1,082 (50·4\\%) were dependent; 3,007 (52.9\\%) reported recent needle sharing. Awareness of HCV positive status was significantly associated with higher education, HIV testing history, awareness of HIV positive status, and higher community antiretroviral therapy coverage.\n\nInterpretation\nThe high burden of HCV and HIV/HCV co-infection coupled with low-access to HCV services highlights an urgent need to include RLS in the global HCV agenda. While newer treatments will become available globally in the near future, programs to improve awareness, and reduce disease progression and transmission need to be scaled-up without further delay. Failure to do so could result in patterns of rising mortality, undermining advances in survival attributed to widespread HIV treatment.\n\nFunding\nUS National Institutes of Health},\n\tnumber = {1},\n\turldate = {2017-03-13},\n\tjournal = {The Lancet. Infectious diseases},\n\tauthor = {Solomon, Sunil Suhas and Mehta, Shruti H and Srikrishnan, Aylur K and Solomon, Suniti and McFall, Allison M. and Laeyendecker, Oliver and Celentano, David D and Iqbal, Syed H and Anand, Santhanam and Vasudevan, Canjeevaram K and Saravanan, Shanmugam and Lucas, Gregory M and Kumar, Muniratnam S and Sulkowski, Mark S and Quinn, Thomas C},\n\tmonth = jan,\n\tyear = {2015},\n\tpmid = {25486851},\n\tpmcid = {PMC4503257},\n\tpages = {36--45},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n Background Globally, 90% of HCV-infected individuals reside in resource-limited settings (RLS). We characterized the prevalence of HCV, HIV/HCV co-infection, and the HCV care continuum among people who inject drugs (PWID) in India. Methods 14,481 PWID were sampled from 15 cities throughout India using respondent-driven sampling (RDS) from January–December 2013. HCV prevalence was estimated by the presence of anti-HCV antibodies incorporating RDS weights. HCV care continuum outcomes were self-reported except for viral clearance among treatment-experienced participants. Findings Median age was 30 years and 13,608/14,449 (92·4%) were male. Overall weighted HCV prevalence was 37·2% (5,777/14,447); HIV/HCV co-infection prevalence was 13·2% (2,085/14,435). Correlates of HCV infection included higher lifetime injection frequency, HIV positivity, and a higher prevalence of persons with HIV RNA \\textgreater 1000 copies/ml in the community. Of 5,777 HCV antibody positive PWID, 440 (5·5%) were aware of their status, 225 (3·0%) had seen a doctor for their HCV, 79 (1·4%) had taken HCV treatment, and 18 (0·4%) had undetectable HCV RNA. Overall, 6,138/12,128 (50·5%) did not get tested for HCV because they had never heard of HCV. Among the 5,777 HCV antibody positives, 2,086 (34·4%) reported harmful/hazardous alcohol use of whom 1,082 (50·4%) were dependent; 3,007 (52.9%) reported recent needle sharing. Awareness of HCV positive status was significantly associated with higher education, HIV testing history, awareness of HIV positive status, and higher community antiretroviral therapy coverage. Interpretation The high burden of HCV and HIV/HCV co-infection coupled with low-access to HCV services highlights an urgent need to include RLS in the global HCV agenda. While newer treatments will become available globally in the near future, programs to improve awareness, and reduce disease progression and transmission need to be scaled-up without further delay. Failure to do so could result in patterns of rising mortality, undermining advances in survival attributed to widespread HIV treatment. Funding US National Institutes of Health\n

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\n \n\n \n \n Mehta, S. H.; Lucas, G. M.; Solomon, S.; Srikrishnan, A. K.; McFall, A. M.; Dhingra, N.; Nandagopal, P.; Kumar, M. S.; Celentano, D. D.; and Solomon, S. S.\n\n\n \n \n \n \n \n HIV Care Continuum Among Men Who Have Sex With Men and Persons Who Inject Drugs in India: Barriers to Successful Engagement.\n \n \n \n \n\n\n \n\n\n\n Clinical Infectious Diseases: An Official Publication of the Infectious Diseases Society of America, 61(11): 1732–1741. December 2015.\n \n\n\n\n
\n\n\n\n \n \n $\"HIV$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{mehta_hiv_2015,\n\ttitle = {{HIV} {Care} {Continuum} {Among} {Men} {Who} {Have} {Sex} {With} {Men} and {Persons} {Who} {Inject} {Drugs} in {India}: {Barriers} to {Successful} {Engagement}},\n\tvolume = {61},\n\tissn = {1058-4838},\n\tshorttitle = {{HIV} {Care} {Continuum} {Among} {Men} {Who} {Have} {Sex} {With} {Men} and {Persons} {Who} {Inject} {Drugs} in {India}},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4643485/},\n\tdoi = {10.1093/cid/civ669},\n\tabstract = {We characterized the human immunodeficiency virus (HIV) care continuum among men who have sex with men and persons who inject drugs across 27 sites in India. The primary barrier to engagement was awareness of HIV-positive status., Background. We characterize the human immunodeficiency virus (HIV) care continuum for men who have sex with men (MSM) and persons who inject drugs (PWID) across India., Methods. We recruited 12 022 MSM and 14 481 PWID across 26 Indian cities, using respondent-driven sampling (September 2012 to December 2013). Participants were aged ≥18 years and either self-identified as male and reported sex with a man in the prior year (MSM) or reported injection drug use in the prior 2 years (PWID). Correlates of awareness of HIV-positive status were characterized using multilevel logistic regression., Results. A total of 1146 MSM were HIV infected, of whom a median of 30\\% were aware of their HIV-positive status, 23\\% were linked to care, 22\\% were retained before antiretroviral therapy (ART), 16\\% had started ART, 16\\% were currently receiving ART, and 10\\% had suppressed viral loads. There was site variability (awareness range, 0\\%–90\\%; suppressed viral load range, 0\\%–58\\%). A total of 2906 PWID were HIV infected, of whom a median of 41\\% were aware, 36\\% were linked to care, 31\\% were retained before ART, 20\\% had started ART, 18\\% were currently receiving ART, and 15\\% had suppressed viral loads. Similar site variability was observed (awareness range: 2\\%–93\\%; suppressed viral load range: 0\\%–47\\%). Factors significantly associated with awareness were region, older age, being married (MSM) or female (PWID), use of other services (PWID), more lifetime sexual partners (MSM), and needle sharing (PWID). Ongoing injection drug use (PWID) and alcohol use (MSM) were associated with lower awareness., Conclusions. In this large sample, the major barrier to HIV care engagement was awareness of HIV-positive status. Efforts should focus on linking HIV testing to other essential services., Clinical Trials Registration. NCT01686750.},\n\tnumber = {11},\n\turldate = {2017-03-13},\n\tjournal = {Clinical Infectious Diseases: An Official Publication of the Infectious Diseases Society of America},\n\tauthor = {Mehta, Shruti H. and Lucas, Gregory M. and Solomon, Suniti and Srikrishnan, Aylur K. and McFall, Allison M. and Dhingra, Neeraj and Nandagopal, Paneerselvam and Kumar, M. Suresh and Celentano, David D. and Solomon, Sunil S.},\n\tmonth = dec,\n\tyear = {2015},\n\tpmid = {26251048},\n\tpmcid = {PMC4643485},\n\tpages = {1732--1741},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n We characterized the human immunodeficiency virus (HIV) care continuum among men who have sex with men and persons who inject drugs across 27 sites in India. The primary barrier to engagement was awareness of HIV-positive status., Background. We characterize the human immunodeficiency virus (HIV) care continuum for men who have sex with men (MSM) and persons who inject drugs (PWID) across India., Methods. We recruited 12 022 MSM and 14 481 PWID across 26 Indian cities, using respondent-driven sampling (September 2012 to December 2013). Participants were aged ≥18 years and either self-identified as male and reported sex with a man in the prior year (MSM) or reported injection drug use in the prior 2 years (PWID). Correlates of awareness of HIV-positive status were characterized using multilevel logistic regression., Results. A total of 1146 MSM were HIV infected, of whom a median of 30% were aware of their HIV-positive status, 23% were linked to care, 22% were retained before antiretroviral therapy (ART), 16% had started ART, 16% were currently receiving ART, and 10% had suppressed viral loads. There was site variability (awareness range, 0%–90%; suppressed viral load range, 0%–58%). A total of 2906 PWID were HIV infected, of whom a median of 41% were aware, 36% were linked to care, 31% were retained before ART, 20% had started ART, 18% were currently receiving ART, and 15% had suppressed viral loads. Similar site variability was observed (awareness range: 2%–93%; suppressed viral load range: 0%–47%). Factors significantly associated with awareness were region, older age, being married (MSM) or female (PWID), use of other services (PWID), more lifetime sexual partners (MSM), and needle sharing (PWID). Ongoing injection drug use (PWID) and alcohol use (MSM) were associated with lower awareness., Conclusions. In this large sample, the major barrier to HIV care engagement was awareness of HIV-positive status. Efforts should focus on linking HIV testing to other essential services., Clinical Trials Registration. NCT01686750.\n

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\n \n\n \n \n Lucas, G. M.; Solomon, S. S.; Srikrishnan, A. K.; Agrawal, A.; Iqbal, S.; Laeyendecker, O.; McFall, A. M.; Kumar, M. S.; Ogburn, E.; Celentano, D. D.; Solomon, S.; and Mehta, S. H.\n\n\n \n \n \n \n \n High HIV burden among people who inject drugs in 15 Indian cities.\n \n \n \n \n\n\n \n\n\n\n AIDS (London, England), 29(5): 619–628. March 2015.\n \n\n\n\n
\n\n\n\n \n \n $\"High$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{lucas_high_2015,\n\ttitle = {High {HIV} burden among people who inject drugs in 15 {Indian} cities},\n\tvolume = {29},\n\tissn = {0269-9370},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4346289/},\n\tdoi = {10.1097/QAD.0000000000000592},\n\tabstract = {Background\nInjecting drug use has historically been the principal driver of the HIV epidemic in the Northeast states of India. However, recent data indicate growing numbers of people who inject drugs (PWID) in North and Central Indian cities.\n\nMethods\nWe conducted face-to-face surveys among PWID in 7 Northeast and 8 North/Central Indian cities using respondent-driven sampling. We used a rapid HIV testing protocol to identify seropositive individuals and multi-assay algorithm to identify those with recent infection. We used multi-level regression models that incorporated sampling weights and had random intercepts for site to assess risk factors for prevalent and incident (recent) HIV infection.\n\nResults\nWe surveyed 14,481 PWID from 15 Indian cities between January and December 2013. Participants reported high rates of needle/syringe sharing. The median (site range) estimated HIV prevalence and incidence were 18.1\\% (5.9, 44.9) and 2.9 per 100 person-years (0, 12.4), respectively. HIV prevalence was higher in Northeast sites while HIV incidence was higher in North/Central sites. The odds of prevalent HIV were over 3-fold higher in women than men. Other factors associated with HIV prevalence or incidence included duration since first injection, injection of pharmaceutical drugs, and needle/syringe sharing.\n\nConclusions\nThe burden of HIV infection is high among PWID in India, and may be increasing in cities where injecting drug use is emerging. Women who inject drugs were at substantially higher risk for HIV than men, a situation that may be mediated by dual injection-related and sexual risks.},\n\tnumber = {5},\n\turldate = {2017-03-13},\n\tjournal = {AIDS (London, England)},\n\tauthor = {Lucas, Gregory M. and Solomon, Sunil S. and Srikrishnan, Aylur K. and Agrawal, Alok and Iqbal, Syed and Laeyendecker, Oliver and McFall, Allison M. and Kumar, Muniratnam S. and Ogburn, Elizabeth and Celentano, David D. and Solomon, Suniti and Mehta, Shruti H.},\n\tmonth = mar,\n\tyear = {2015},\n\tpmid = {25715105},\n\tpmcid = {PMC4346289},\n\tpages = {619--628},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Kurth, A. E.; Cleland, C. M.; Des Jarlais, D. C.; Musyoki, H.; Lizcano, J. A.; Chhun, N.; and Cherutich, P.\n\n\n \n \n \n \n \n HIV prevalence, estimated incidence, and risk behaviors among people who inject drugs in Kenya.\n \n \n \n \n\n\n \n\n\n\n Journal of acquired immune deficiency syndromes (1999), 70(4): 420–427. December 2015.\n \n\n\n\n
\n\n\n\n \n \n $\"HIV$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{kurth_hiv_2015,\n\ttitle = {{HIV} prevalence, estimated incidence, and risk behaviors among people who inject drugs in {Kenya}},\n\tvolume = {70},\n\tissn = {1525-4135},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4624615/},\n\tdoi = {10.1097/QAI.0000000000000769},\n\tabstract = {Objective\nHIV infection in sub-Saharan Africa increasingly occurs among people who inject drugs (PWID). Kenya is one of the first to implement a national needle and syringe program (NSP). Our study undertook a baseline assessment as part of evaluating NSP in a seek, test, treat, and retain approach.\n\nMethods\nParticipants enrolled May–December 2012 from 10 sites. Respondent-driven sampling was used to reach n=1,785 PWID for HIV-1 prevalence and viral load determination and survey data.\n\nResults\nEstimated HIV prevalence, adjusted for differential network size and recruitment relationships, was 14.5\\% in Nairobi (95\\% CI 10.8–18.2) and 20.5\\% in the Coast region (95\\% CI 17.3–23.6). Viral load (log10 transformed) in Nairobi ranged from 1.71 to 6.12 (median 4.41; IQR 3.51–4.94) and in the Coast from 1.71 to 5.88 (median 4.01; IQR 3.44–4.72). Using log10 viral load 2.6 as a threshold for HIV viral suppression, the percentage of HIV-infected participants with viral suppression was 4.2\\% in Nairobi and 4.6\\% in the Coast. Heroin was the most commonly injected drug in both regions, used by 93\\% of participantsin the past month typically injecting 2–3 times/day. Receptive needle/syringe sharing at last injection was more common in Nairobi (23\\%) than the Coast (4\\%). Estimated incidence among new injectors was 2.5/100 person-years in Nairobi and 1.6/100 person-years in the Coast.\n\nConclusion\nThe HIV epidemic is well-established among PWID in both Nairobi and Coast regions. Public health scale implementation of combination HIV prevention has the potential to greatly limit the epidemic in this vulnerable and bridging population.},\n\tnumber = {4},\n\turldate = {2017-03-13},\n\tjournal = {Journal of acquired immune deficiency syndromes (1999)},\n\tauthor = {Kurth, Ann E. and Cleland, Charles M. and Des Jarlais, Don C. and Musyoki, Helgar and Lizcano, John A. and Chhun, Nok and Cherutich, Peter},\n\tmonth = dec,\n\tyear = {2015},\n\tpmid = {26226249},\n\tpmcid = {PMC4624615},\n\tpages = {420--427},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Hammett, T. M.; Donahue, S.; LeRoy, L.; Montague, B. T.; Rosen, D. L.; Solomon, L.; Costa, M.; Wohl, D.; and Rich, J. D.\n\n\n \n \n \n \n \n Transitions to Care in the Community for Prison Releasees with HIV: a Qualitative Study of Facilitators and Challenges in Two States.\n \n \n \n \n\n\n \n\n\n\n Journal of Urban Health : Bulletin of the New York Academy of Medicine, 92(4): 650–666. August 2015.\n \n\n\n\n
\n\n\n\n \n \n $\"Transitions$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{hammett_transitions_2015,\n\ttitle = {Transitions to {Care} in the {Community} for {Prison} {Releasees} with {HIV}: a {Qualitative} {Study} of {Facilitators} and {Challenges} in {Two} {States}},\n\tvolume = {92},\n\tissn = {1099-3460},\n\tshorttitle = {Transitions to {Care} in the {Community} for {Prison} {Releasees} with {HIV}},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4524841/},\n\tdoi = {10.1007/s11524-015-9968-x},\n\tabstract = {One in seven people living with HIV in the USA passes through a prison or jail each year, and almost all will return to the community. Discharge planning and transitional programs are critical but challenging elements in ensuring continuity of care, maintaining treatment outcomes achieved in prison, and preventing further viral transmission. This paper describes facilitators and challenges of in-prison care, transitional interventions, and access to and continuity of care in the community in Rhode Island and North Carolina based on qualitative data gathered as part of the mixed-methods Link Into Care Study of prisoners and releasees with HIV. We conducted 65 interviews with correctional and community-based providers and administrators and analyzed the transcripts using NVivo 10 to identify major themes. Facilitators of effective transitional systems in both states included the following: health providers affiliated with academic institutions or other entities independent of the corrections department; organizational philosophy emphasizing a patient-centered, personal, and holistic approach; strong leadership with effective “champions”; a team approach with coordination, collaboration and integration throughout the system, mutual respect and learning between corrections and health providers, staff dedicated to transitional services, and effective communication and information sharing among providers; comprehensive transitional activities and services including HIV, mental health and substance use services in prisons, timely and comprehensive discharge planning with specific linkages/appointments, supplies of medications on release, access to benefits and entitlements, case management and proactive follow-up on missed appointments; and releasees’ commitment to transitional plans. These elements were generally present in both study states but their absence, which also sometimes occurred, represent ongoing challenges to success. The qualitative findings on the facilitators and challenges of the transitional systems were similar in the two states despite differences in context, demographics of target population, and system organization. Recommendations for improved transitional systems follow from the analysis of the facilitators and challenges.},\n\tnumber = {4},\n\turldate = {2017-03-13},\n\tjournal = {Journal of Urban Health : Bulletin of the New York Academy of Medicine},\n\tauthor = {Hammett, Theodore M. and Donahue, Sara and LeRoy, Lisa and Montague, Brian T. and Rosen, David L. and Solomon, Liza and Costa, Michael and Wohl, David and Rich, Josiah D.},\n\tmonth = aug,\n\tyear = {2015},\n\tpmid = {26022666},\n\tpmcid = {PMC4524841},\n\tpages = {650--666},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n One in seven people living with HIV in the USA passes through a prison or jail each year, and almost all will return to the community. Discharge planning and transitional programs are critical but challenging elements in ensuring continuity of care, maintaining treatment outcomes achieved in prison, and preventing further viral transmission. This paper describes facilitators and challenges of in-prison care, transitional interventions, and access to and continuity of care in the community in Rhode Island and North Carolina based on qualitative data gathered as part of the mixed-methods Link Into Care Study of prisoners and releasees with HIV. We conducted 65 interviews with correctional and community-based providers and administrators and analyzed the transcripts using NVivo 10 to identify major themes. Facilitators of effective transitional systems in both states included the following: health providers affiliated with academic institutions or other entities independent of the corrections department; organizational philosophy emphasizing a patient-centered, personal, and holistic approach; strong leadership with effective “champions”; a team approach with coordination, collaboration and integration throughout the system, mutual respect and learning between corrections and health providers, staff dedicated to transitional services, and effective communication and information sharing among providers; comprehensive transitional activities and services including HIV, mental health and substance use services in prisons, timely and comprehensive discharge planning with specific linkages/appointments, supplies of medications on release, access to benefits and entitlements, case management and proactive follow-up on missed appointments; and releasees’ commitment to transitional plans. These elements were generally present in both study states but their absence, which also sometimes occurred, represent ongoing challenges to success. The qualitative findings on the facilitators and challenges of the transitional systems were similar in the two states despite differences in context, demographics of target population, and system organization. Recommendations for improved transitional systems follow from the analysis of the facilitators and challenges.\n

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\n \n\n \n \n Gwadz, M.; Cleland, C. M.; Leonard, N. R.; Kutnick, A.; Ritchie, A. S.; Banfield, A.; Hagan, H.; Perlman, D. C.; McCright-Gill, T.; Sherpa, D.; and Martinez, B. Y.\n\n\n \n \n \n \n \n Hybrid STTR intervention for heterosexuals using anonymous HIV testing and confidential linkage to care: a single arm exploratory trial using respondent-driven sampling.\n \n \n \n \n\n\n \n\n\n\n BMC Public Health, 15. November 2015.\n \n\n\n\n
\n\n\n\n \n \n $\"Hybrid$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{gwadz_hybrid_2015,\n\ttitle = {Hybrid {STTR} intervention for heterosexuals using anonymous {HIV} testing and confidential linkage to care: a single arm exploratory trial using respondent-driven sampling},\n\tvolume = {15},\n\tissn = {1471-2458},\n\tshorttitle = {Hybrid {STTR} intervention for heterosexuals using anonymous {HIV} testing and confidential linkage to care},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4647497/},\n\tdoi = {10.1186/s12889-015-2451-5},\n\tabstract = {Background\nAn estimated 14 \\% of the 1.2 million individuals living with HIV in the U.S. are unaware of their status. Yet this modest proportion of individuals with undiagnosed HIV is linked to 44–66 \\% of all new infections. Thus innovative intervention approaches are needed to seek out and test those with undiagnosed HIV, and link them to HIV treatment with high retention, an approach referred to as “Seek, Test, Treat, and Retain” (STTR). The present protocol describes a creative “hybrid” STTR approach that uses anonymous HIV testing followed by confidential care linkage, focused on heterosexuals at high risk (HHR) for HIV, who do not test as frequently as, and are diagnosed later, than other risk groups.\n\nMethods/Design\nThis is a single-arm exploratory intervention efficacy trial. The study has two phases: one to seek out and test HHR, and another to link those found infected to HIV treatment in a timely fashion, with high retention. We will recruit African American/Black and Latino adult HHR who reside in urban locations with high poverty and HIV prevalence. Participants will be recruited with respondent-driven sampling, a peer recruitment method. The “Seek and Test” phase is comprised of a brief, convenient, single-session, anonymous HIV counseling and testing session. The “Treat and Retain” component will engage those newly diagnosed with HIV into a confidential research phase and use a set of procedures called care navigation to link them to HIV primary care. Participants will be followed for 6 months with objective assessment of outcomes (using medical records and biomarkers).\n\nDiscussion\nUndiagnosed HIV infection is a major public health problem. While anonymous HIV testing is an important part of the HIV testing portfolio, it does not typically include linkage to care. The present study has potential to produce an innovative, brief, cost-effective, and replicable STTR intervention, and thereby reduce racial/ethnic disparities in HIV/AIDS.\n\nTrial Registration\nClinicalTrials.gov, NCT02421159, Registered April 15, 2015.},\n\turldate = {2017-03-13},\n\tjournal = {BMC Public Health},\n\tauthor = {Gwadz, Marya and Cleland, Charles M. and Leonard, Noelle R. and Kutnick, Alexandra and Ritchie, Amanda S. and Banfield, Angela and Hagan, Holly and Perlman, David C. and McCright-Gill, Talaya and Sherpa, Dawa and Martinez, Belkis Y.},\n\tmonth = nov,\n\tyear = {2015},\n\tpmid = {26572865},\n\tpmcid = {PMC4647497},\n}\n\n\n\n\n\n\n\n\n\n\n\n

\n\n\n

\n Background An estimated 14 % of the 1.2 million individuals living with HIV in the U.S. are unaware of their status. Yet this modest proportion of individuals with undiagnosed HIV is linked to 44–66 % of all new infections. Thus innovative intervention approaches are needed to seek out and test those with undiagnosed HIV, and link them to HIV treatment with high retention, an approach referred to as “Seek, Test, Treat, and Retain” (STTR). The present protocol describes a creative “hybrid” STTR approach that uses anonymous HIV testing followed by confidential care linkage, focused on heterosexuals at high risk (HHR) for HIV, who do not test as frequently as, and are diagnosed later, than other risk groups. Methods/Design This is a single-arm exploratory intervention efficacy trial. The study has two phases: one to seek out and test HHR, and another to link those found infected to HIV treatment in a timely fashion, with high retention. We will recruit African American/Black and Latino adult HHR who reside in urban locations with high poverty and HIV prevalence. Participants will be recruited with respondent-driven sampling, a peer recruitment method. The “Seek and Test” phase is comprised of a brief, convenient, single-session, anonymous HIV counseling and testing session. The “Treat and Retain” component will engage those newly diagnosed with HIV into a confidential research phase and use a set of procedures called care navigation to link them to HIV primary care. Participants will be followed for 6 months with objective assessment of outcomes (using medical records and biomarkers). Discussion Undiagnosed HIV infection is a major public health problem. While anonymous HIV testing is an important part of the HIV testing portfolio, it does not typically include linkage to care. The present study has potential to produce an innovative, brief, cost-effective, and replicable STTR intervention, and thereby reduce racial/ethnic disparities in HIV/AIDS. Trial Registration ClinicalTrials.gov, NCT02421159, Registered April 15, 2015.\n

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\n \n\n \n \n Gwadz, M.; Cleland, C. M.; Hagan, H.; Jenness, S.; Kutnick, A.; Leonard, N. R.; Applegate, E.; Ritchie, A. S.; Banfield, A.; Belkin, M.; Cross, B.; Del Olmo, M.; Ha, K.; Martinez, B. Y.; McCright-Gill, T.; Swain, Q. L.; Perlman, D. C.; and Kurth, A. E.\n\n\n \n \n \n \n \n Strategies to uncover undiagnosed HIV infection among heterosexuals at high risk and link them to HIV care with high retention: a “seek, test, treat, and retain” study.\n \n \n \n \n\n\n \n\n\n\n BMC Public Health, 15. May 2015.\n \n\n\n\n
\n\n\n\n \n \n $\"Strategies$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{gwadz_strategies_2015,\n\ttitle = {Strategies to uncover undiagnosed {HIV} infection among heterosexuals at high risk and link them to {HIV} care with high retention: a “seek, test, treat, and retain” study},\n\tvolume = {15},\n\tissn = {1471-2458},\n\tshorttitle = {Strategies to uncover undiagnosed {HIV} infection among heterosexuals at high risk and link them to {HIV} care with high retention},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4434577/},\n\tdoi = {10.1186/s12889-015-1816-0},\n\tabstract = {Background\nOver 50,000 individuals become infected with HIV annually in the U.S., and over a quarter of HIV infected individuals are heterosexuals. Undiagnosed HIV infection, as well as a lack of retention in care among those diagnosed, are both primary factors contributing to ongoing HIV incidence. Further, there are racial/ethnic disparities in undiagnosed HIV and engagement in care, with African Americans/Blacks and Latinos remaining undiagnosed longer and less engaged in care than Whites, signaling the need for culturally targeted intervention approaches to seek and test those with undiagnosed HIV infection, and link them to care with high retention.\n\nMethods/Design\nThe study has two components: one to seek out and test heterosexuals at high risk for HIV infection, and another to link those found infected to HIV care with high retention. We will recruit sexually active African American/Black and Latino adults who have opposite sex partners, negative or unknown HIV status, and reside in locations with high poverty and HIV prevalence. The “Seek and Test” component will compare the efficacy and cost effectiveness of two strategies to uncover undiagnosed HIV infection: venue-based sampling and respondent-driven sampling (RDS). Among those recruited by RDS and found to have HIV infection, a “Treat and Retain” component will assess the efficacy of a peer-driven intervention compared to a control arm with respect to time to an HIV care appointment and health indicators using a cluster randomized controlled trial design to minimize contamination. RDS initial seeds will be randomly assigned to the intervention or control arm at a 1:1 ratio and all recruits will be assigned to the same arm as the recruiter. Participants will be followed for 12 months with outcomes assessed using medical records and biomarkers, such as HIV viral load.\n\nDiscussion\nHeterosexuals do not test for HIV as frequently as and are diagnosed later than other risk groups. The study has the potential to contribute an efficient, innovative, and sustainable multi-level recruitment approach and intervention to the HIV prevention portfolio. Because the majority of heterosexuals at high risk are African American/Black or Latino, the study has great potential to reduce racial/ethnic disparities in HIV/AIDS.\n\nTrial registration\nClinicalTrials.gov, NCT01607541, Registered May 23, 2012.},\n\turldate = {2017-03-13},\n\tjournal = {BMC Public Health},\n\tauthor = {Gwadz, Marya and Cleland, Charles M. and Hagan, Holly and Jenness, Samuel and Kutnick, Alexandra and Leonard, Noelle R. and Applegate, Elizabeth and Ritchie, Amanda S. and Banfield, Angela and Belkin, Mindy and Cross, Bridget and Del Olmo, Montserrat and Ha, Katharine and Martinez, Belkis Y. and McCright-Gill, Talaya and Swain, Quentin L. and Perlman, David C. and Kurth, Ann E.},\n\tmonth = may,\n\tyear = {2015},\n\tpmid = {25958200},\n\tpmcid = {PMC4434577},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n Background Over 50,000 individuals become infected with HIV annually in the U.S., and over a quarter of HIV infected individuals are heterosexuals. Undiagnosed HIV infection, as well as a lack of retention in care among those diagnosed, are both primary factors contributing to ongoing HIV incidence. Further, there are racial/ethnic disparities in undiagnosed HIV and engagement in care, with African Americans/Blacks and Latinos remaining undiagnosed longer and less engaged in care than Whites, signaling the need for culturally targeted intervention approaches to seek and test those with undiagnosed HIV infection, and link them to care with high retention. Methods/Design The study has two components: one to seek out and test heterosexuals at high risk for HIV infection, and another to link those found infected to HIV care with high retention. We will recruit sexually active African American/Black and Latino adults who have opposite sex partners, negative or unknown HIV status, and reside in locations with high poverty and HIV prevalence. The “Seek and Test” component will compare the efficacy and cost effectiveness of two strategies to uncover undiagnosed HIV infection: venue-based sampling and respondent-driven sampling (RDS). Among those recruited by RDS and found to have HIV infection, a “Treat and Retain” component will assess the efficacy of a peer-driven intervention compared to a control arm with respect to time to an HIV care appointment and health indicators using a cluster randomized controlled trial design to minimize contamination. RDS initial seeds will be randomly assigned to the intervention or control arm at a 1:1 ratio and all recruits will be assigned to the same arm as the recruiter. Participants will be followed for 12 months with outcomes assessed using medical records and biomarkers, such as HIV viral load. Discussion Heterosexuals do not test for HIV as frequently as and are diagnosed later than other risk groups. The study has the potential to contribute an efficient, innovative, and sustainable multi-level recruitment approach and intervention to the HIV prevention portfolio. Because the majority of heterosexuals at high risk are African American/Black or Latino, the study has great potential to reduce racial/ethnic disparities in HIV/AIDS. Trial registration ClinicalTrials.gov, NCT01607541, Registered May 23, 2012.\n

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\n \n\n \n \n Beckwith, C. G.; Kurth, A. E.; Bazerman, L.; Solomon, L.; Patry, E.; Rich, J. D.; and Kuo, I.\n\n\n \n \n \n \n \n Survey of US Correctional Institutions for Routine HCV Testing.\n \n \n \n \n\n\n \n\n\n\n American Journal of Public Health, 105(1): 68–71. January 2015.\n \n\n\n\n
\n\n\n\n \n \n $\"Survey$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{beckwith_survey_2015,\n\ttitle = {Survey of {US} {Correctional} {Institutions} for {Routine} {HCV} {Testing}},\n\tvolume = {105},\n\tissn = {0090-0036},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4265939/},\n\tdoi = {10.2105/AJPH.2014.302071},\n\tabstract = {To ascertain HCV testing practices among US prisons and jails, we conducted a survey study in 2012, consisting of medical directors of all US state prisons and 40 of the largest US jails, that demonstrated a minority of US prisons and jails conduct routine HCV testing. Routine voluntary HCV testing in correctional facilities is urgently needed to increase diagnosis, enable risk-reduction counseling and preventive health care, and facilitate evaluation for antiviral treatment.},\n\tnumber = {1},\n\turldate = {2017-03-13},\n\tjournal = {American Journal of Public Health},\n\tauthor = {Beckwith, Curt G. and Kurth, Ann E. and Bazerman, Lauri and Solomon, Liza and Patry, Emily and Rich, Josiah D. and Kuo, Irene},\n\tmonth = jan,\n\tyear = {2015},\n\tpmid = {25393180},\n\tpmcid = {PMC4265939},\n\tpages = {68--71},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Kitahata, M. M.; Drozd, D. R.; Crane, H. M.; Van Rompaey, S. E.; Althoff, K. N.; Gange, S. J.; Klein, M. B.; Lucas, G. M.; Abraham, A. G.; Lo Re, V.; McReynolds, J.; Lober, W. B.; Mendes, A.; Modur, S. P.; Jing, Y.; Morton, E. J.; Griffith, M. A.; Freeman, A. M.; and Moore, R. D.\n\n\n \n \n \n \n Ascertainment and verification of end-stage renal disease and end-stage liver disease in the north american AIDS cohort collaboration on research and design.\n \n \n \n\n\n \n\n\n\n AIDS research and treatment, 2015: 923194. 2015.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{kitahata_ascertainment_2015,\n\ttitle = {Ascertainment and verification of end-stage renal disease and end-stage liver disease in the north american {AIDS} cohort collaboration on research and design},\n\tvolume = {2015},\n\tissn = {2090-1240},\n\tdoi = {10.1155/2015/923194},\n\tabstract = {The burden of HIV disease has shifted from traditional AIDS-defining illnesses to serious non-AIDS-defining comorbid conditions. Research aimed at improving HIV-related comorbid disease outcomes requires well-defined, verified clinical endpoints. We developed methods to ascertain and verify end-stage renal disease (ESRD) and end-stage liver disease (ESLD) and validated screening algorithms within the largest HIV cohort collaboration in North America (NA-ACCORD). Individuals who screened positive among all participants in twelve cohorts enrolled between January 1996 and December 2009 underwent medical record review to verify incident ESRD or ESLD using standardized protocols. We randomly sampled 6\\% of contributing cohorts to determine the sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of ESLD and ESRD screening algorithms in a validation subcohort. Among 43,433 patients screened for ESRD, 822 screened positive of which 620 met clinical criteria for ESRD. The algorithm had 100\\% sensitivity, 99\\% specificity, 82\\% PPV, and 100\\% NPV for ESRD. Among 41,463 patients screened for ESLD, 2,024 screened positive of which 645 met diagnostic criteria for ESLD. The algorithm had 100\\% sensitivity, 95\\% specificity, 27\\% PPV, and 100\\% NPV for ESLD. Our methods proved robust for ascertainment of ESRD and ESLD in persons infected with HIV.},\n\tlanguage = {eng},\n\tjournal = {AIDS research and treatment},\n\tauthor = {Kitahata, Mari M. and Drozd, Daniel R. and Crane, Heidi M. and Van Rompaey, Stephen E. and Althoff, Keri N. and Gange, Stephen J. and Klein, Marina B. and Lucas, Gregory M. and Abraham, Alison G. and Lo Re, Vincent and McReynolds, Justin and Lober, William B. and Mendes, Adell and Modur, Sharada P. and Jing, Yuezhou and Morton, Elizabeth J. and Griffith, Margaret A. and Freeman, Aimee M. and Moore, Richard D.},\n\tyear = {2015},\n\tpmid = {25789171},\n\tpmcid = {PMC4350581},\n\tpages = {923194},\n}\n\n\n\n\n\n\n\n

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\n \n\n \n \n Comfort, M.; Lopez, A. M.; Powers, C.; Kral, A. H.; and Lorvick, J.\n\n\n \n \n \n \n \n How Institutions Deprive: Ethnography, Social Work, and Interventionist Ethics Among the Hypermarginalized.\n \n \n \n \n\n\n \n\n\n\n The Russell Sage Foundation Journal of the Social Sciences, 1(1): 100–119. November 2015.\n \n\n\n\n
\n\n\n\n \n \n $\"How$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{comfort_how_2015,\n\ttitle = {How {Institutions} {Deprive}: {Ethnography}, {Social} {Work}, and {Interventionist} {Ethics} {Among} the {Hypermarginalized}.},\n\tvolume = {1},\n\turl = {http://www.rsfjournal.org/doi/full/10.7758/RSF.2015.1.1.06},\n\tabstract = {Hypermarginalized populations, such as homeless drug users with acute health problems, are subject to multiple intersecting adversities that result in social exclusion and chronic suffering. Despite this population's high need for health and social services, institutions provide services that are fragmented and often punitive, contributing to further marginality. In this article, we present a hybrid methodological approach that combines clinical social work and ethnography in a study of intensive case management for HIV-positive indigent adults in Oakland, California. We investigate two primary research questions. First, we consider the challenges this population faces in navigating institutions to meet their basic needs, and we demonstrate how organizational irrationality has severe consequences for this population. Second, we grapple with the question of how to ethically engage hypermarginalized participants in research by presenting a clinically informed intervention that is responsive to individual vulnerabilities and also enhances our understanding of institutional failure.},\n\tnumber = {1},\n\tjournal = {The Russell Sage Foundation Journal of the Social Sciences},\n\tauthor = {Comfort, Megan and Lopez, Andrea M. and Powers, Christina and Kral, Alex H. and Lorvick, Jennifer},\n\tmonth = nov,\n\tyear = {2015},\n\tkeywords = {ethnography, incarceration, poverty, research methods, social work},\n\tpages = {100--119},\n}\n\n\n\n\n\n\n\n\n

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\n \n 2014\n \n \n (8)\n \n \n

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\n \n\n \n \n Sanger, P.; Hartzler, A.; Lober, W. B.; Evans, H. L.; and Pratt, W.\n\n\n \n \n \n \n Design Considerations for Post-Acute Care mHealth: Patient Perspectives.\n \n \n \n\n\n \n\n\n\n AMIA ... Annual Symposium proceedings / AMIA Symposium. AMIA Symposium, 2014: 1920–1929. 2014.\n \n\n\n\n
\n\n\n\n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{sanger_design_2014,\n\ttitle = {Design {Considerations} for {Post}-{Acute} {Care} {mHealth}: {Patient} {Perspectives}},\n\tvolume = {2014},\n\tissn = {1942-597X},\n\tshorttitle = {Design {Considerations} for {Post}-{Acute} {Care} {mHealth}},\n\tabstract = {Many current mobile health applications ("apps") and most previous research have been directed at management of chronic illnesses. However, little is known about patient preferences and design considerations for apps intended to help in a post-acute setting. Our team is developing an mHealth platform to engage patients in wound tracking to identify and manage surgical site infections (SSI) after hospital discharge. Post-discharge SSIs are a major source of morbidity and expense, and occur at a critical care transition when patients are physically and emotionally stressed. Through interviews with surgical patients who experienced SSI, we derived design considerations for such a post-acute care app. Key design qualities include: meeting basic accessibility, usability and security needs; encouraging patient-centeredness; facilitating better, more predictable communication; and supporting personalized management by providers. We illustrate our application of these guiding design considerations and propose a new framework for mHealth design based on illness duration and intensity.},\n\tlanguage = {eng},\n\tjournal = {AMIA ... Annual Symposium proceedings / AMIA Symposium. AMIA Symposium},\n\tauthor = {Sanger, Patrick and Hartzler, Andrea and Lober, William B. and Evans, Heather L. and Pratt, Wanda},\n\tyear = {2014},\n\tpmid = {25954465},\n\tpmcid = {PMC4419922},\n\tkeywords = {Acute Disease, Adult, Aged, Attitude to Health, Continuity of Patient Care, Female, Humans, Male, Middle Aged, Mobile Applications, Patient Discharge, Self Care, Telemedicine, surgical wound infection},\n\tpages = {1920--1929},\n}\n\n\n\n\n\n\n\n

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\n \n\n \n \n Young, J. D.; Patel, M.; Badowski, M.; Mackesy-Amiti, M. E.; Vaughn, P.; Shicker, L.; Puisis, M.; and Ouellet, L. J.\n\n\n \n \n \n \n \n Improved Virologic Suppression With HIV Subspecialty Care in a Large Prison System Using Telemedicine: An Observational Study With Historical Controls.\n \n \n \n \n\n\n \n\n\n\n Clinical Infectious Diseases: An Official Publication of the Infectious Diseases Society of America, 59(1): 123–126. July 2014.\n \n\n\n\n
\n\n\n\n \n \n $\"Improved$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{young_improved_2014,\n\ttitle = {Improved {Virologic} {Suppression} {With} {HIV} {Subspecialty} {Care} in a {Large} {Prison} {System} {Using} {Telemedicine}: {An} {Observational} {Study} {With} {Historical} {Controls}},\n\tvolume = {59},\n\tissn = {1058-4838},\n\tshorttitle = {Improved {Virologic} {Suppression} {With} {HIV} {Subspecialty} {Care} in a {Large} {Prison} {System} {Using} {Telemedicine}},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4305134/},\n\tdoi = {10.1093/cid/ciu222},\n\tabstract = {Correctional populations have an elevated human immunodeficiency virus (HIV) prevalence, yet many individuals lack access to subspecialty care. Our study showed that HIV-infected inmates had significantly greater virologic suppression and higher CD4 T-lymphocyte counts when managed by a multidisciplinary team of subspecialists conducting clinics via telemedicine. In other studies, these outcomes have been associated with reductions on HIV-related morbidity and mortality, as well as HIV transmission.},\n\tnumber = {1},\n\turldate = {2017-03-13},\n\tjournal = {Clinical Infectious Diseases: An Official Publication of the Infectious Diseases Society of America},\n\tauthor = {Young, Jeremy D. and Patel, Mahesh and Badowski, Melissa and Mackesy-Amiti, Mary Ellen and Vaughn, Pyrai and Shicker, Louis and Puisis, Michael and Ouellet, Lawrence J.},\n\tmonth = jul,\n\tyear = {2014},\n\tpmid = {24723283},\n\tpmcid = {PMC4305134},\n\tpages = {123--126},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Wechsberg, W. M; Zule, W. A; Ndirangu, J.; Kline, T. L; Rodman, N. F; Doherty, I. A; Novak, S. P; and van der Horst, C. M\n\n\n \n \n \n \n \n The biobehavioral Women’s Health CoOp in Pretoria, South Africa: study protocol for a cluster-randomized design.\n \n \n \n \n\n\n \n\n\n\n BMC Public Health, 14. October 2014.\n \n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{wechsberg_biobehavioral_2014,\n\ttitle = {The biobehavioral {Women}’s {Health} {CoOp} in {Pretoria}, {South} {Africa}: study protocol for a cluster-randomized design},\n\tvolume = {14},\n\tissn = {1471-2458},\n\tshorttitle = {The biobehavioral {Women}’s {Health} {CoOp} in {Pretoria}, {South} {Africa}},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4287508/},\n\tdoi = {10.1186/1471-2458-14-1074},\n\tabstract = {Background\nSouth Africa has 6.4 million adults over the age of 15 living with HIV. Gender inequality issues continue to drive the HIV epidemic in South Africa, where Black African women bear the greatest HIV burden. Limited access to services; little capacity to negotiate sex and condom use; and other legal, social, and economic inequities make women highly vulnerable to HIV infection. Behavioral interventions have been shown to decrease risk behaviors, but they have been less successful in reducing HIV incidence. Conversely, biomedical prevention strategies have proven to be successful in reducing HIV incidence, but require behavioral interventions to increase uptake and adherence. Consequently, there is a need for integrated approaches that combine biomedical and behavioral interventions. Effective combination prevention efforts should comprise biomedical, behavioral, and structural programming proven in randomized trials that focuses on the driving forces and key populations at higher risk of HIV infection and transmission.\n\nMethods/Design\nThis prospective, geographically clustered randomized field experiment is enrolling participants into two arms: a control arm that receives standard HIV testing and referral for treatment; and an intervention arm that receives an evidence-based, woman-focused behavioral intervention that emphasizes risk reduction and retention, the Women’s Health CoOp. We divided the city of Pretoria into 14 mutually exclusive geographic zones and randomized these zones into either the control arm or the intervention arm. Outreach workers are recruiting drug-using women from each zone. At baseline, eligible participants complete a questionnaire and biological testing for HIV, recent drug use, and pregnancy. Follow-up interviews are completed at 6 and 12 months.\n\nDiscussion\nThe biobehavioral intervention in this study merges an efficacious behavioral HIV prevention intervention for women with biomedical prevention through HIV treatment as prevention using a Seek, Test, Treat and Retain strategy. This combination biobehavioral intervention is designed to (1) improve the quality of life and reduce HIV infectiousness among women who are HIV positive, and (2) reduce HIV risk behaviors among women regardless of their HIV status. If efficacious, this intervention could help control the HIV epidemic in South Africa.\n\nTrial registration\nTrial registration no: NCT01497405.},\n\turldate = {2017-03-13},\n\tjournal = {BMC Public Health},\n\tauthor = {Wechsberg, Wendee M and Zule, William A and Ndirangu, Jacqueline and Kline, Tracy L and Rodman, Nathaniel F and Doherty, Irene A and Novak, Scott P and van der Horst, Charles M},\n\tmonth = oct,\n\tyear = {2014},\n\tpmid = {25318563},\n\tpmcid = {PMC4287508},\n}\n\n\n\n\n\n\n\n\n\n\n\n

\n\n\n

\n Background South Africa has 6.4 million adults over the age of 15 living with HIV. Gender inequality issues continue to drive the HIV epidemic in South Africa, where Black African women bear the greatest HIV burden. Limited access to services; little capacity to negotiate sex and condom use; and other legal, social, and economic inequities make women highly vulnerable to HIV infection. Behavioral interventions have been shown to decrease risk behaviors, but they have been less successful in reducing HIV incidence. Conversely, biomedical prevention strategies have proven to be successful in reducing HIV incidence, but require behavioral interventions to increase uptake and adherence. Consequently, there is a need for integrated approaches that combine biomedical and behavioral interventions. Effective combination prevention efforts should comprise biomedical, behavioral, and structural programming proven in randomized trials that focuses on the driving forces and key populations at higher risk of HIV infection and transmission. Methods/Design This prospective, geographically clustered randomized field experiment is enrolling participants into two arms: a control arm that receives standard HIV testing and referral for treatment; and an intervention arm that receives an evidence-based, woman-focused behavioral intervention that emphasizes risk reduction and retention, the Women’s Health CoOp. We divided the city of Pretoria into 14 mutually exclusive geographic zones and randomized these zones into either the control arm or the intervention arm. Outreach workers are recruiting drug-using women from each zone. At baseline, eligible participants complete a questionnaire and biological testing for HIV, recent drug use, and pregnancy. Follow-up interviews are completed at 6 and 12 months. Discussion The biobehavioral intervention in this study merges an efficacious behavioral HIV prevention intervention for women with biomedical prevention through HIV treatment as prevention using a Seek, Test, Treat and Retain strategy. This combination biobehavioral intervention is designed to (1) improve the quality of life and reduce HIV infectiousness among women who are HIV positive, and (2) reduce HIV risk behaviors among women regardless of their HIV status. If efficacious, this intervention could help control the HIV epidemic in South Africa. Trial registration Trial registration no: NCT01497405.\n

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\n \n\n \n \n Tomori, C.; Go, V. F.; Tuan, L. N.; Huong, N. M.; Binh, N. T.; Zelaya, C. E.; Celentano, D. D.; Dat, D. T.; and Quan, V. M.\n\n\n \n \n \n \n \n “In their perception we are addicts”: Social vulnerabilities and sources of support for men released from drug treatment centers in Vietnam.\n \n \n \n \n\n\n \n\n\n\n The International journal on drug policy, 25(5): 897–904. September 2014.\n \n\n\n\n
\n\n\n\n \n \n $\"“In$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{tomori_their_2014,\n\ttitle = {“{In} their perception we are addicts”: {Social} vulnerabilities and sources of support for men released from drug treatment centers in {Vietnam}},\n\tvolume = {25},\n\tissn = {0955-3959},\n\tshorttitle = {“{In} their perception we are addicts”},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4205961/},\n\tdoi = {10.1016/j.drugpo.2014.04.012},\n\tabstract = {Background\nAmid the global transition to treat opioid addiction as an illness, many people who inject drugs (PWID) face heterogeneous legal environments that include both punitive and harm reduction measures. In Vietnam, many PWID, who have a high burden of HIV, are sent to drug treatment centers, or “06 centers”, for compulsory detoxification, vocational training, and labor for up to four years. This study investigates the challenges and facilitators of reentry into community and family life among men who are released from “06 centers” and provides insights and recommendations for developing policies and interventions that address special needs of this vulnerable population.\n\nMethods\nIn-depth interviews were conducted in 2011 by trained interviewers among a sample of 43 male PWID released within the past 2 years from “06 centers” in Hanoi, Vietnam to investigate the above issues and to recommend potential interventions. Participants were recruited from outpatient HIV clinics that serve PWID (n=22) and through peer referral from self-help groups for PWID (n=21). Interviews were audiotaped, transcribed, translated, entered into Atlas. TI qualitative data analysis software and analyzed for key themes.\n\nResults\nThe interviews revealed persistent drug-related stigmatization, frequently paired with HIV-related stigmatization and discrimination, which hindered employment, increased participants’ social isolation and exacerbated their struggles with addiction. Families were participants’ primary source of financial, employment, and emotional support, but addiction-related family tensions also had negative psychological effects. Participants identified methadone maintenance treatment as an effective means of overcoming addiction, yet few could fully benefit from this treatment due to its limited availability.\n\nConclusion\nOur study suggests that PWID released from “06 centers” would greatly benefit from the scale-up of community-based harm reduction measures that include addiction and HIV treatment, coupled with employment-support and family-centered mental health services.},\n\tnumber = {5},\n\turldate = {2017-03-13},\n\tjournal = {The International journal on drug policy},\n\tauthor = {Tomori, Cecilia and Go, Vivian F. and Tuan, Le Nhan and Huong, Nguyen Mai and Binh, Nguyen Thanh and Zelaya, Carla E. and Celentano, David D. and Dat, Do Tuan and Quan, Vu Minh},\n\tmonth = sep,\n\tyear = {2014},\n\tpmid = {24857185},\n\tpmcid = {PMC4205961},\n\tpages = {897--904},\n}\n\n\n\n\n\n\n\n\n\n\n\n

\n\n\n

\n Background Amid the global transition to treat opioid addiction as an illness, many people who inject drugs (PWID) face heterogeneous legal environments that include both punitive and harm reduction measures. In Vietnam, many PWID, who have a high burden of HIV, are sent to drug treatment centers, or “06 centers”, for compulsory detoxification, vocational training, and labor for up to four years. This study investigates the challenges and facilitators of reentry into community and family life among men who are released from “06 centers” and provides insights and recommendations for developing policies and interventions that address special needs of this vulnerable population. Methods In-depth interviews were conducted in 2011 by trained interviewers among a sample of 43 male PWID released within the past 2 years from “06 centers” in Hanoi, Vietnam to investigate the above issues and to recommend potential interventions. Participants were recruited from outpatient HIV clinics that serve PWID (n=22) and through peer referral from self-help groups for PWID (n=21). Interviews were audiotaped, transcribed, translated, entered into Atlas. TI qualitative data analysis software and analyzed for key themes. Results The interviews revealed persistent drug-related stigmatization, frequently paired with HIV-related stigmatization and discrimination, which hindered employment, increased participants’ social isolation and exacerbated their struggles with addiction. Families were participants’ primary source of financial, employment, and emotional support, but addiction-related family tensions also had negative psychological effects. Participants identified methadone maintenance treatment as an effective means of overcoming addiction, yet few could fully benefit from this treatment due to its limited availability. Conclusion Our study suggests that PWID released from “06 centers” would greatly benefit from the scale-up of community-based harm reduction measures that include addiction and HIV treatment, coupled with employment-support and family-centered mental health services.\n

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\n \n\n \n \n Solomon, L.; Montague, B. T.; Beckwith, C. G.; Baillargeon, J.; Costa, M.; Dumont, D.; Kuo, I.; Kurth, A.; and Rich, J. D.\n\n\n \n \n \n \n \n Survey Finds That Many Prisons And Jails Have Room To Improve HIV Testing And Coordination Of Postrelease Treatment.\n \n \n \n \n\n\n \n\n\n\n Health affairs (Project Hope), 33(3): 434–442. March 2014.\n \n\n\n\n
\n\n\n\n \n \n $\"Survey$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{solomon_survey_2014,\n\ttitle = {Survey {Finds} {That} {Many} {Prisons} {And} {Jails} {Have} {Room} {To} {Improve} {HIV} {Testing} {And} {Coordination} {Of} {Postrelease} {Treatment}},\n\tvolume = {33},\n\tissn = {0278-2715},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4028701/},\n\tdoi = {10.1377/hlthaff.2013.1115},\n\tabstract = {Early diagnosis of HIV and effective antiretroviral treatment are key elements in efforts to reduce the morbidity and mortality associated with HIV. Incarcerated populations are disproportionately affected by HIV, with the disease’s prevalence among inmates estimated to be three to five times higher than among the general population. Correctional institutions offer important opportunities to test for HIV and link infected people to postrelease treatment services. To examine HIV testing and policies that help HIV-positive people obtain treatment in the community after release, we administered a survey to the medical directors of the fifty state prison systems and of forty of the largest jails in the United States. We found that 19 percent of prison systems and 35 percent of jails provide opt-out HIV testing, which is recommended by the Centers for Disease Control and Prevention (CDC). Additionally, fewer than 20 percent of prisons and jails conform to the CDC’s recommendations regarding discharge planning services for inmates transitioning to the community: making an appointment with a community health care provider, assisting with enrollment in an entitlement program, and providing a copy of the medical record and a supply of HIV medications. These findings suggest that opportunities for HIV diagnosis and linking HIV-positive inmates to community care after release are being missed in the majority of prison systems and jails.},\n\tnumber = {3},\n\turldate = {2017-03-13},\n\tjournal = {Health affairs (Project Hope)},\n\tauthor = {Solomon, Liza and Montague, Brian T. and Beckwith, Curt G. and Baillargeon, Jacques and Costa, Michael and Dumont, Dora and Kuo, Irene and Kurth, Ann and Rich, Josiah D.},\n\tmonth = mar,\n\tyear = {2014},\n\tpmid = {24590942},\n\tpmcid = {PMC4028701},\n\tpages = {434--442},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Di Paola, A.; Lincoln, T.; Skiest, D. J.; Desabrais, M.; Altice, F. L.; and Springer, S. A.\n\n\n \n \n \n \n \n Design and methods of a double blind randomized placebo-controlled trial of extended-release naltrexone for HIV-infected, opioid dependent prisoners and jail detainees who are transitioning to the community.\n \n \n \n \n\n\n \n\n\n\n Contemporary clinical trials, 39(2): 256–268. November 2014.\n \n\n\n\n
\n\n\n\n \n \n $\"Design$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{di_paola_design_2014,\n\ttitle = {Design and methods of a double blind randomized placebo-controlled trial of extended-release naltrexone for {HIV}-infected, opioid dependent prisoners and jail detainees who are transitioning to the community},\n\tvolume = {39},\n\tissn = {1551-7144},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4283549/},\n\tdoi = {10.1016/j.cct.2014.09.002},\n\tabstract = {Background\nPeople with opioid dependence and HIV are concentrated within criminal justice settings (CJS). Upon release, however, drug relapse is common and contributes to poor HIV treatment outcomes, increased HIV transmission risk, reincarceration and mortality. Extended-release naltrexone (XR-NTX) is an evidence-based treatment for opioid dependence, yet is not routinely available for CJS populations.\n\nMethods\nA randomized, double-blind, placebo-controlled trial of XR-NTX for HIV-infected inmates transitioning from correctional to community settings is underway to assess its impact on HIV and opioid-relapse outcomes.\n\nResults\nWe describe the methods and early acceptability of this trial. In addition we provide protocol details to safely administer XR-NTX near community release and describe logistical implementation issues identified. Study acceptability was modest, with 132 (66\\%) persons who consented to participate from 199 total referrals. Overall, 79\\% of the participants had previously received opioid agonist treatment before this incarceration. Thus far, 65 (49\\%) of those agreeing to participate in the trial have initiated XR-NTX or placebo. Of the 134 referred patients who ultimately did not receive a first injection, the main reasons included a preference for an alternative opioid agonist treatment (37\\%), being ineligible (32\\%), not yet released (10\\%), and lost upon release before an receiving their injection (14\\%).\n\nConclusions\nStudy findings should provide high internal validity about HIV and opioid treatment outcomes for HIV-infected prisoners transitioning to the community. The large number of patients who ultimately did not receive the study medication may raise external validity concerns due to XR-NTX acceptability and interest in opioid agonist treatments.},\n\tnumber = {2},\n\turldate = {2017-03-13},\n\tjournal = {Contemporary clinical trials},\n\tauthor = {Di Paola, Angela and Lincoln, Thomas and Skiest, Daniel J. and Desabrais, Maureen and Altice, Frederick L. and Springer, Sandra A.},\n\tmonth = nov,\n\tyear = {2014},\n\tpmid = {25240704},\n\tpmcid = {PMC4283549},\n\tpages = {256--268},\n}\n\n\n\n\n\n\n\n

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\n \n\n \n \n Christopoulos, K. A; Riley, E. D; Tulsky, J.; Carrico, A. W; Moskowitz, J. T; Wilson, L.; Coffin, L. S; Falahati, V.; Akerley, J.; and Hilton, J. F\n\n\n \n \n \n \n \n A text messaging intervention to improve retention in care and virologic suppression in a U.S. urban safety-net HIV clinic: study protocol for the Connect4Care (C4C) randomized controlled trial.\n \n \n \n \n\n\n \n\n\n\n BMC Infectious Diseases, 14. December 2014.\n \n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{christopoulos_text_2014,\n\ttitle = {A text messaging intervention to improve retention in care and virologic suppression in a {U}.{S}. urban safety-net {HIV} clinic: study protocol for the {Connect4Care} ({C4C}) randomized controlled trial},\n\tvolume = {14},\n\tissn = {1471-2334},\n\tshorttitle = {A text messaging intervention to improve retention in care and virologic suppression in a {U}.{S}. urban safety-net {HIV} clinic},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4323139/},\n\tdoi = {10.1186/s12879-014-0718-6},\n\tabstract = {Background\nFew data exist on the use of text messaging as a tool to promote retention in HIV care and virologic suppression at the clinic level in the United States. We describe the protocol for a study designed to investigate whether a text messaging intervention that supports healthy behaviors, encourages consistent engagement with care, and promotes antiretroviral persistence can improve retention in care and virologic suppression among patients in an urban safety-net HIV clinic in San Francisco.\n\nMethods/Design\nConnect4Care (C4C) is a single-site, randomized year-long study of text message appointment reminders vs. text message appointment reminders plus thrice-weekly supportive, informational, and motivational text messages. Eligible consenting patients are allocated 1:1 to the two arms within strata defined by HIV diagnosis within the past 12 months (i.e. “newly diagnosed”) vs. earlier. Study participants must receive primary care at the San Francisco General Hospital HIV clinic, speak English, possess a cell phone and be willing to send/receive up to 25 text messages per month, a have viral load {\\textgreater}200 copies/μL, and be either new to the clinic or have a history of poor retention. The primary efficacy outcome is virologic suppression at 12 months and the key secondary outcome, which will also be examined as a mediator of the primary outcome, is retention in HIV care, as operationalized by kept and missed primary care visits. Process outcomes include text message response rate and percent of time in study without cell phone service. Generalized estimating equation log-binomial models will be used for intent to treat, per protocol, and mediation analyses. An assessment of the cost and cost-effectiveness of the intervention is planned along with a qualitative evaluation of the intervention.\n\nDiscussion\nFindings from this study will provide valuable information about the use of behavioral-theory based text messaging to promote retention in HIV care and virologic suppression, further elucidate the challenges of using texting technology with marginalized urban populations, and help guide the development of new mobile health strategies to improve HIV care cascade outcomes.\n\nTrial registration\n\n            NCT01917994\n          \n\nElectronic supplementary material\nThe online version of this article (doi:10.1186/s12879-014-0718-6) contains supplementary material, which is available to authorized users.},\n\turldate = {2017-03-13},\n\tjournal = {BMC Infectious Diseases},\n\tauthor = {Christopoulos, Katerina A and Riley, Elise D and Tulsky, Jacqueline and Carrico, Adam W and Moskowitz, Judith T and Wilson, Leslie and Coffin, Lara S and Falahati, Veesta and Akerley, Jordan and Hilton, Joan F},\n\tmonth = dec,\n\tyear = {2014},\n\tpmid = {25551175},\n\tpmcid = {PMC4323139},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

\n\n\n

\n Background Few data exist on the use of text messaging as a tool to promote retention in HIV care and virologic suppression at the clinic level in the United States. We describe the protocol for a study designed to investigate whether a text messaging intervention that supports healthy behaviors, encourages consistent engagement with care, and promotes antiretroviral persistence can improve retention in care and virologic suppression among patients in an urban safety-net HIV clinic in San Francisco. Methods/Design Connect4Care (C4C) is a single-site, randomized year-long study of text message appointment reminders vs. text message appointment reminders plus thrice-weekly supportive, informational, and motivational text messages. Eligible consenting patients are allocated 1:1 to the two arms within strata defined by HIV diagnosis within the past 12 months (i.e. “newly diagnosed”) vs. earlier. Study participants must receive primary care at the San Francisco General Hospital HIV clinic, speak English, possess a cell phone and be willing to send/receive up to 25 text messages per month, a have viral load \\textgreater200 copies/μL, and be either new to the clinic or have a history of poor retention. The primary efficacy outcome is virologic suppression at 12 months and the key secondary outcome, which will also be examined as a mediator of the primary outcome, is retention in HIV care, as operationalized by kept and missed primary care visits. Process outcomes include text message response rate and percent of time in study without cell phone service. Generalized estimating equation log-binomial models will be used for intent to treat, per protocol, and mediation analyses. An assessment of the cost and cost-effectiveness of the intervention is planned along with a qualitative evaluation of the intervention. Discussion Findings from this study will provide valuable information about the use of behavioral-theory based text messaging to promote retention in HIV care and virologic suppression, further elucidate the challenges of using texting technology with marginalized urban populations, and help guide the development of new mobile health strategies to improve HIV care cascade outcomes. Trial registration NCT01917994 Electronic supplementary material The online version of this article (doi:10.1186/s12879-014-0718-6) contains supplementary material, which is available to authorized users.\n

\n\n\n

\n \n\n \n \n Di Paola, A.; Lincoln, T.; Skiest, D. J.; Desabrais, M.; Altice, F. L.; and Springer, S. A.\n\n\n \n \n \n \n Design and methods of a double blind randomized placebo-controlled trial of extended-release naltrexone for HIV-infected, opioid dependent prisoners and jail detainees who are transitioning to the community.\n \n \n \n\n\n \n\n\n\n Contemporary Clinical Trials, 39(2): 256–268. November 2014.\n \n\n\n\n
\n\n\n\n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n\n\n

@article{di_paola_design_2014,\n\ttitle = {Design and methods of a double blind randomized placebo-controlled trial of extended-release naltrexone for {HIV}-infected, opioid dependent prisoners and jail detainees who are transitioning to the community},\n\tvolume = {39},\n\tissn = {1559-2030},\n\tdoi = {10.1016/j.cct.2014.09.002},\n\tabstract = {BACKGROUND: People with opioid dependence and HIV are concentrated within criminal justice settings (CJS). Upon release, however, drug relapse is common and contributes to poor HIV treatment outcomes, increased HIV transmission risk, reincarceration and mortality. Extended-release naltrexone (XR-NTX) is an evidence-based treatment for opioid dependence, yet is not routinely available for CJS populations.\nMETHODS: A randomized, double-blind, placebo-controlled trial of XR-NTX for HIV-infected inmates transitioning from correctional to community settings is underway to assess its impact on HIV and opioid-relapse outcomes.\nRESULTS: We describe the methods and early acceptability of this trial. In addition we provide protocol details to safely administer XR-NTX near community release and describe logistical implementation issues identified. Study acceptability was modest, with 132 (66\\%) persons who consented to participate from 199 total referrals. Overall, 79\\% of the participants had previously received opioid agonist treatment before this incarceration. Thus far, 65 (49\\%) of those agreeing to participate in the trial have initiated XR-NTX or placebo. Of the 134 referred patients who ultimately did not receive a first injection, the main reasons included a preference for an alternative opioid agonist treatment (37\\%), being ineligible (32\\%), not yet released (10\\%), and lost upon release before receiving their injection (14\\%).\nCONCLUSIONS: Study findings should provide high internal validity about HIV and opioid treatment outcomes for HIV-infected prisoners transitioning to the community. The large number of patients who ultimately did not receive the study medication may raise external validity concerns due to XR-NTX acceptability and interest in opioid agonist treatments.\nCLINICAL TRIAL NUMBER: NCT01246401.},\n\tlanguage = {eng},\n\tnumber = {2},\n\tjournal = {Contemporary Clinical Trials},\n\tauthor = {Di Paola, Angela and Lincoln, Thomas and Skiest, Daniel J. and Desabrais, Maureen and Altice, Frederick L. and Springer, Sandra A.},\n\tmonth = nov,\n\tyear = {2014},\n\tpmid = {25240704},\n\tpmcid = {PMC4283549},\n\tkeywords = {Communication, Delayed-Action Preparations, Double-Blind Method, Extended-release naltrexone, Female, HIV, HIV Infections, Humans, Injections, Intramuscular, Male, Naltrexone, Narcotic Antagonists, Opioid dependence, Opioid-Related Disorders, Patient Compliance, Prisoners, Randomized controlled trial, Research Design, Risk-Taking, Time Factors, Vivitrol},\n\tpages = {256--268},\n}\n\n\n\n\n\n\n\n

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\n \n 2013\n \n \n (3)\n \n \n

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\n \n\n \n \n Solomon, S. S.; Lucas, G. M.; Celentano, D. D.; Sifakis, F.; and Mehta, S. H.\n\n\n \n \n \n \n \n Beyond Surveillance: A Role for Respondent-driven Sampling in Implementation Science.\n \n \n \n \n\n\n \n\n\n\n American Journal of Epidemiology, 178(2): 260–267. July 2013.\n \n\n\n\n
\n\n\n\n \n \n $\"Beyond$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{solomon_beyond_2013,\n\ttitle = {Beyond {Surveillance}: {A} {Role} for {Respondent}-driven {Sampling} in {Implementation} {Science}},\n\tvolume = {178},\n\tissn = {0002-9262},\n\tshorttitle = {Beyond {Surveillance}},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3712656/},\n\tdoi = {10.1093/aje/kws432},\n\tabstract = {We are now in the fourth decade of the human immunodeficiency virus (HIV) pandemic. Several novel prevention tools have been identified, and prevalence and incidence have declined in many settings. A remaining challenge is the delivery of preventive interventions to hard-to-reach populations, including men who have sex with men and injection drug users. Leaders in the field of HIV have called for a new focus on implementation science, which requires a shift in thinking from individual randomized controlled trials to cluster-randomized trials. Multiple challenges need to be addressed in the conduct of cluster-randomized trials, including: 1) generalizability of the study population to the target population, 2) potential contamination through overlap/exchange of members of control and intervention clusters, and 3) evaluation of effectiveness at multiple levels of influence. To address these key challenges, we propose a novel application of respondent-driven sampling—a chain-referral strategy commonly used for surveillance—in the recruitment of participants for the evaluation of a cluster-randomized trial of a community intervention. We illustrate this application with an empirical example of a cluster-randomized trial that is currently under way to assess the effectiveness of men's wellness centers in improving utilization of HIV counseling and testing among men who have sex with men in India.},\n\tnumber = {2},\n\turldate = {2017-03-13},\n\tjournal = {American Journal of Epidemiology},\n\tauthor = {Solomon, Sunil S. and Lucas, Gregory M. and Celentano, David D. and Sifakis, Frangiscos and Mehta, Shruti H.},\n\tmonth = jul,\n\tyear = {2013},\n\tpmid = {23801014},\n\tpmcid = {PMC3712656},\n\tpages = {260--267},\n}\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Kurth, A.; Kuo, I.; Peterson, J.; Azikiwe, N.; Bazerman, L.; Cates, A.; and Beckwith, C. G.\n\n\n \n \n \n \n \n Information and Communication Technology to Link Criminal Justice Reentrants to HIV Care in the Community.\n \n \n \n \n\n\n \n\n\n\n AIDS Research and Treatment, 2013. 2013.\n \n\n\n\n
\n\n\n\n \n \n $\"Information$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{kurth_information_2013,\n\ttitle = {Information and {Communication} {Technology} to {Link} {Criminal} {Justice} {Reentrants} to {HIV} {Care} in the {Community}},\n\tvolume = {2013},\n\tissn = {2090-1240},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3745938/},\n\tdoi = {10.1155/2013/547381},\n\tabstract = {The United States has the world's highest prison population, and an estimated one in seven HIV-positive persons in the USA passes through a correctional facility annually. Given this, it is critical to develop innovative and effective approaches to support HIV treatment and retention in care among HIV-positive individuals involved in the criminal justice (CJ) system. Information and communication technologies (ICTs), including mobile health (mHealth) interventions, may offer one component of a successful strategy for linkage/retention in care. We describe CARE+ Corrections, a randomized controlled trial (RCT) study now underway in Washington, that will evaluate the combined effect of computerized motivational interview counseling and postrelease short message service (SMS) text message reminders to increase antiretroviral therapy (ART) adherence and linkage and retention in care among HIV-infected persons involved in the criminal justice system. In this report, we describe the development of this ICT/mHealth intervention, outline the study procedures used to evaluate this intervention, and summarize the implications for the mHealth knowledge base.},\n\turldate = {2017-03-13},\n\tjournal = {AIDS Research and Treatment},\n\tauthor = {Kurth, Ann and Kuo, Irene and Peterson, James and Azikiwe, Nkiru and Bazerman, Lauri and Cates, Alice and Beckwith, Curt G.},\n\tyear = {2013},\n\tpmid = {23984054},\n\tpmcid = {PMC3745938},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n\n \n \n Gordon, M. S.; Kinlock, T. W.; McKenzie, M.; Wilson, M. E.; and Rich, J. D.\n\n\n \n \n \n \n \n Rapid HIV Testing for Individuals on Probation/Parole: Outcomes of an Intervention Trial.\n \n \n \n \n\n\n \n\n\n\n AIDS and behavior, 17(6): 2022–2030. July 2013.\n \n\n\n\n
\n\n\n\n \n \n $\"Rapid$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{gordon_rapid_2013,\n\ttitle = {Rapid {HIV} {Testing} for {Individuals} on {Probation}/{Parole}: {Outcomes} of an {Intervention} {Trial}},\n\tvolume = {17},\n\tissn = {1090-7165},\n\tshorttitle = {Rapid {HIV} {Testing} for {Individuals} on {Probation}/{Parole}},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3674156/},\n\tdoi = {10.1007/s10461-013-0456-6},\n\tabstract = {Many probationers and parolees do not receive HIV testing despite being at increased risk for obtaining and transmitting HIV. A two-group randomized controlled trial was conducted between April, 2011 and May, 2012 at probation/parole offices in Baltimore, Maryland and Providence/Pawtucket, Rhode Island. Male and female probationers/parolees were interviewed (N=1263) and then offered HIV testing based on random assignment to one of two conditions: 1) On-site rapid HIV testing conducted at the probation/parole office; or 2) Referral for rapid HIV testing off site at a community HIV testing clinic. Outcomes were: 1) undergoing HIV testing; and 2) receipt of HIV testing results. Participants were significantly more likely to be tested onsite at a probation/parole office versus off-site at a HIV testing clinic (p {\\textless} .001). There was no difference between the two groups in terms of receiving HIV testing results. Findings indicate that probationers/ parolees are willing to be tested on-site and, independent of testing location, are equally willing to receive their results. Implications for expanding rapid HIV testing to more criminal justice related locations and populations are discussed.},\n\tnumber = {6},\n\turldate = {2017-03-13},\n\tjournal = {AIDS and behavior},\n\tauthor = {Gordon, Michael S. and Kinlock, Timothy W. and McKenzie, Michelle and Wilson, Monique E. and Rich, Josiah D.},\n\tmonth = jul,\n\tyear = {2013},\n\tpmid = {23536140},\n\tpmcid = {PMC3674156},\n\tpages = {2022--2030},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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\n \n 2012\n \n \n (2)\n \n \n

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\n \n\n \n \n Montague, B. T.; Rosen, D. L.; Solomon, L.; Nunn, A.; Green, T.; Costa, M.; Baillargeon, J.; Wohl, D. A.; Paar, D. P.; Rich, J. D.; and Study Group, o. b. o. t. L.\n\n\n \n \n \n \n \n Tracking linkage to HIV care for former prisoners.\n \n \n \n \n\n\n \n\n\n\n Virulence, 3(3): 319–324. May 2012.\n \n\n\n\n
\n\n\n\n \n \n $\"Tracking$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{montague_tracking_2012,\n\ttitle = {Tracking linkage to {HIV} care for former prisoners},\n\tvolume = {3},\n\tissn = {2150-5594},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3442844/},\n\tdoi = {10.4161/viru.20432},\n\tabstract = {Improving testing and uptake to care among highly impacted populations is a critical element of Seek, Test, Treat and Retain strategies for reducing HIV incidence in the community. HIV disproportionately impacts prisoners. Though, incarceration provides an opportunity to diagnose and initiate therapy, treatment is frequently disrupted after release. Though model programs exist to support linkage to care on release, there is a lack of scalable metrics with which to assess adequacy of linkage to care after release. The linking data from Ryan White program Client Level Data (CLD) files reported to HRSA with corrections release data offers an attractive means of generating these metrics. Identified only by use of a confidential encrypted Unique Client Identifier (eUCI) these CLD files allow collection of key clinical indicators across the system of Ryan White funded providers. Using eUCIs generated from corrections release data sets as a linkage tool, the time to the first service at community providers along with key clinical indicators of patient status at entry into care can be determined as measures of linkage adequacy. Using this strategy, high and low performing sites can be identified and best practices can be identified to reproduce these successes in other settings.},\n\tnumber = {3},\n\turldate = {2017-03-13},\n\tjournal = {Virulence},\n\tauthor = {Montague, Brian T. and Rosen, David L. and Solomon, Liza and Nunn, Amy and Green, Traci and Costa, Michael and Baillargeon, Jacques and Wohl, David A. and Paar, David P. and Rich, Josiah D. and Study Group, on behalf of the LINCS},\n\tmonth = may,\n\tyear = {2012},\n\tpmid = {22561157},\n\tpmcid = {PMC3442844},\n\tpages = {319--324},\n}\n\n\n\n

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\n \n\n \n \n Knight, K; and Flynn, P\n\n\n \n \n \n \n \n Clinical trials involving prisoners: a bioethical perspective.\n \n \n \n \n\n\n \n\n\n\n Clin. Invest., 12(2): 1147–1149. 2012.\n \n\n\n\n
\n\n\n\n \n \n $\"Clinical$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{knight_clinical_2012,\n\ttitle = {Clinical trials involving prisoners: a bioethical perspective.},\n\tvolume = {12},\n\tissn = {2041-6792},\n\turl = {http://www.openaccessjournals.com/articles/clinical-trials-involving-prisoners-a-bioethical-perspective.pdf},\n\tnumber = {2},\n\tjournal = {Clin. Invest.},\n\tauthor = {Knight, K and Flynn, P},\n\tyear = {2012},\n\tpages = {1147--1149},\n}\n\n\n\n\n\n\n\n

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\n \n 2011\n \n \n (1)\n \n \n

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\n \n\n \n \n Yokell, M. A.; Green, T. C.; Bowman, S.; McKenzie, M.; and Rich, J. D.\n\n\n \n \n \n \n \n Opioid Overdose Prevention and Naloxone Distribution in Rhode Island.\n \n \n \n \n\n\n \n\n\n\n Medicine and health, Rhode Island, 94(8): 240–242. August 2011.\n \n\n\n\n
\n\n\n\n \n \n $\"Opioid$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@article{yokell_opioid_2011,\n\ttitle = {Opioid {Overdose} {Prevention} and {Naloxone} {Distribution} in {Rhode} {Island}},\n\tvolume = {94},\n\tissn = {1086-5462},\n\turl = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3177423/},\n\tnumber = {8},\n\turldate = {2017-03-13},\n\tjournal = {Medicine and health, Rhode Island},\n\tauthor = {Yokell, Michael A. and Green, Traci C. and Bowman, Sarah and McKenzie, Michelle and Rich, Josiah D.},\n\tmonth = aug,\n\tyear = {2011},\n\tpmid = {21913619},\n\tpmcid = {PMC3177423},\n\tpages = {240--242},\n}\n\n\n\n\n\n\n\n\n\n\n\n

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